Relevant bibliographies by topics / Monociti

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Academic literature on the topic 'Monociti'

Author: Grafiati
Published: 21 February 2023
Last updated: 9 March 2023

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Journal articles on the topic "Monociti"

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Matarrese, Paola, and Giuseppe Marano. "Modulazione dei recettori β-adrenergici e differenze di genere." CARDIOLOGIA AMBULATORIALE 30, no. 1 (May 31, 2022): 20–24. http://dx.doi.org/10.17473/1971-6818-2022-1-5.

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Lo scompenso cardiaco (SC), processo evolutivo comune di più malattie cardiovascolari a differente eziologia (ad es. infarto del miocardio, ipertensione, cardiomiopatie, disturbi valvolari e altre), è diventato sempre più comune nella popolazione anziana, influenzando drasticamente il tasso di sopravvivenza e la qualità della vita. L’iperattività del sistema nervoso simpatico (SNS) che si associa allo SC determina un aumento delle catecolamine circolanti epinefrina e norepinefrina che, attraverso l’attivazione dei recettori beta-adrenergici (β-AR), svolgono un ruolo critico nella regolazione della funzione del sistema cardiovascolare. Una caratteristica distintiva dello SC è la diminuzione o la desensibilizzazione dei recettori β1-adrenergici (β1-AR) sulla membrana delle cellule cardiache. Le catecolamine e lo stress ossidativo sono coinvolti nella regolazione della densità dei β-AR. Lo stress ossidativo associato alla disfunzione mitocondriale sembra giocare un ruolo importante nella fisiopatologia dello SC. Infatti, una condizione di stress ossidativo è stata osservata sia in pazienti con SC che in modelli animali, e un’eccessiva esposizione a specie reattive dell’ossigeno (ROS) diminuisce l’espressione di β1-AR in cardiomiociti murini, sebbene i meccanismi sottostanti rimangano ancora non chiari. Recentemente, è stato scoperto che il recettore periferico delle benzodiazepine (PBR) svolge un ruolo chiave oltre che nell’energetica cellulare, nella regolazione della fisiologia mitocondriale e dell’equilibrio redox nei cardiomiociti. Nel presente studio, abbiamo valutato gli effetti delle catecolamine e dei ligandi del PBR sulla densità dei β1- e β2-AR nei monociti umani isolati da sangue periferico, che sono noti per esprimere entrambi i β-AR. La densità dei β-AR è stata misurata mediante citometria a flusso utilizzando anticorpi selettivi diretti contro un epitopo extracellulare di β1-AR o β2-AR. Il trattamento dei monociti con benzodiazepine induceva una riduzione della densità del β1-AR, ma non del β2-AR, sulla membrana dei monociti che veniva ripristinata utilizzando [1-(2-chlorophenyl)-N-methyl-(1-meth-ylpropyl)-3 isoquinolinecarboxamide] (PK11195), un antagonista del PBR. Questi risultati suggeriscono un possibile ruolo del PBR nella regolazione della densità del β1-AR proponendo i monociti isolati dal sangue periferico sia come modello in vitro utile per lo studio del sistema recettoriale β-adrenergico che come potenziali biomarcatori di progressione della malattia e risposta alla terapia.
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Cazzato, Luciano, Claudia Citarella, Margherita Casanova, Angela Tullo, Maria Luigia Iaculli, and Vincenza D’Onghia. "La granulocitoaferesi." Giornale di Clinica Nefrologica e Dialisi 25, no. 4_suppl (July 23, 2013): S23—S26. http://dx.doi.org/10.33393/gcnd.2013.1085.

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Rettocolite Ulcerosa e Morbo di Crohn, note come Malattie Infiammatorie Croniche Intestinali, sono largamente diffuse nei paesi occidentali. L'eziologia è multifattoriale e comprende una predisposizione genetica e squilibri immunologici del tratto digerente che attivano il processo flogistico della parete intestinale. La terapia delle Malattie Infiammatorie Intestinali comprende amino salicilati, cortisonici, immunosoppressori, ciclosporina e agenti biologici, farmaci gravati da una grave tossicità a lungo termine e da fenomeni di resistenza. Dal momento che granulociti e monociti attivati, insieme a citochine proinflammatorie e alla deregolazione dell'attività dei linfociti T regolatori (T®), hanno un ruolo cruciale nell'infiammazione cronica intestinale, l'aferesi selettiva dei monociti e dei granulociti, una tecnica che rimuove i leucociti attivati dal sangue in regime di circolazione extracorporea, potrebbe rappresentare un presidio terapeutico sicuro ed efficace. Vari studi multicentrici sull'efficacia terapeutica della granulocitoaferesi hanno dimostrato che questa rappresenta un'opzione sicura per i pazienti resistenti alla terapia farmacologica oppure un trattamento ben tollerato in associazione con protocolli terapeutici tradizionali, capace di indurre periodi di remissione clinica prolungati e una significativa riduzione dell'assunzione di cortisonici. Ulteriori studi sono necessari per definire meglio la frequenza del trattamento, i volumi ematici da processare, la migliore terapia farmacologica da associare alla granulocitoaferesi e la sua efficacia in altre patologie autoimmuni.
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Leitch, Ilia J., Jeremy M. Beaulieu, Mark W. Chase, Andrew R. Leitch, and Michael F. Fay. "Genome Size Dynamics and Evolution in Monocots." Journal of Botany 2010 (June 17, 2010): 1–18. http://dx.doi.org/10.1155/2010/862516.

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Monocot genomic diversity includes striking variation at many levels. This paper compares various genomic characters (e.g., range of chromosome numbers and ploidy levels, occurrence of endopolyploidy, GC content, chromosome packaging and organization, genome size) between monocots and the remaining angiosperms to discern just how distinctive monocot genomes are. One of the most notable features of monocots is their wide range and diversity of genome sizes, including the species with the largest genome so far reported in plants. This genomic character is analysed in greater detail, within a phylogenetic context. By surveying available genome size and chromosome data it is apparent that different monocot orders follow distinctive modes of genome size and chromosome evolution. Further insights into genome size-evolution and dynamics were obtained using statistical modelling approaches to reconstruct the ancestral genome size at key nodes across the monocot phylogenetic tree. Such approaches reveal that while the ancestral genome size of all monocots was small ( pg), there have been several major increases and decreases during monocot evolution. In addition, notable increases in the rates of genome size-evolution were found in Asparagales and Poales compared with other monocot lineages.
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Yáñez, Alberto, Madelena Y. Ng, Nargess Hassanzadeh-Kiabi, and Helen S. Goodridge. "IRF8 acts in lineage-committed rather than oligopotent progenitors to control neutrophil vs monocyte production." Blood 125, no. 9 (February 26, 2015): 1452–59. http://dx.doi.org/10.1182/blood-2014-09-600833.

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Key Points IRF8 does not instruct monocytic lineage specification in oligopotent granulocyte-monocyte progenitors. IRF8 regulates the survival and differentiation of lineage-committed progenitors to promote monocyte and suppress neutrophil production.
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Jansen, J. H., J. C. Kluin-Nelemans, J. Van Damme, G. J. Wientjens, R. Willemze, and W. E. Fibbe. "Interleukin 6 is a permissive factor for monocytic colony formation by human hematopoietic progenitor cells." Journal of Experimental Medicine 175, no. 4 (April 1, 1992): 1151–54. http://dx.doi.org/10.1084/jem.175.4.1151.

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Since monocytes and macrophages that arise during the culture of bone marrow progenitor cells are potential sources of interleukin 6 (IL-6), we investigated whether auto- or paracrine production of this factor is involved in colony formation by normal hematopoietic progenitor cells. We added a polyclonal anti-IL-6 antiserum and a monoclonal anti-IL-6 antibody to cultures of monocyte- and T cell-depleted bone marrow cells. Colony formation was stimulated with granulocyte/monocyte-colony-stimulating factor (GM-CSF), monocyte-CSF, or IL-3. Addition of anti-IL-6 antibody resulted in decreased numbers of monocytic colonies to 40-50% of control values, whereas the numbers of granulocytic colonies were not altered. The inhibitory effect was preserved in cultures of CD34(+)-enriched bone marrow cells. As a second approach, we added a monoclonal antibody directed against the IL-6 receptor to cultures of monocyte- and T cell-depleted bone marrow cells. This antibody almost completely inhibited the growth of monocytic colonies, again without decreasing the number of granulocytic colonies. Finally, the importance of IL-6 in monocytopoiesis was demonstrated in serum-deprived bone marrow cultures: addition of exogenous IL-6 to cultures stimulated with GM-CSF resulted in increased numbers of monocytic colonies. Our results indicate that the permissive presence of IL-6 is required for optimal monocytic colony formation by bone marrow progenitor cells.
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Zhang, D. E., K. Fujioka, C. J. Hetherington, L. H. Shapiro, H. M. Chen, A. T. Look, and D. G. Tenen. "Identification of a region which directs the monocytic activity of the colony-stimulating factor 1 (macrophage colony-stimulating factor) receptor promoter and binds PEBP2/CBF (AML1)." Molecular and Cellular Biology 14, no. 12 (December 1994): 8085–95. http://dx.doi.org/10.1128/mcb.14.12.8085-8095.1994.

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The receptor for the macrophage colony-stimulating factor (or colony-stimulating factor 1 [CSF-1]) is expressed from different promoters in monocytic cells and placental trophoblasts. We have demonstrated that the monocyte-specific expression of the CSF-1 receptor is regulated at the level of transcription by a tissue-specific promoter whose activity is stimulated by the monocyte/B-cell-specific transcription factor PU.1 (D.-E. Zhang, C.J. Hetherington, H.-M. Chen, and D.G. Tenen, Mol. Cell. Biol. 14:373-381, 1994). Here we report that the tissue specificity of this promoter is also mediated by sequences in a region II (bp -88 to -59), which lies 10 bp upstream from the PU.1-binding site. When analyzed by DNase footprinting, region II was protected preferentially in monocytic cells. Electrophoretic mobility shift assays confirmed that region II interacts specifically with nuclear proteins from monocytic cells. Two gel shift complexes (Mono A and Mono B) were formed with separate sequence elements within this region. Competition and supershift experiments indicate that Mono B contains a member of the polyomavirus enhancer-binding protein 2/core-binding factor (PEBP2/CBF) family, which includes the AML1 gene product, while Mono A is a distinct complex preferentially expressed in monocytic cells. Promoter constructs with mutations in these sequence elements were no longer expressed specifically in monocytes. Furthermore, multimerized region II sequence elements enhanced the activity of a heterologous thymidine kinase promoter in monocytic cells but not other cell types tested. These results indicate that the monocyte/B-cell-specific transcription factor PU.1 and the Mono A and Mono B protein complexes act in concert to regulate monocyte-specific transcription of the CSF-1 receptor.
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Zhang, D. E., K. Fujioka, C. J. Hetherington, L. H. Shapiro, H. M. Chen, A. T. Look, and D. G. Tenen. "Identification of a region which directs the monocytic activity of the colony-stimulating factor 1 (macrophage colony-stimulating factor) receptor promoter and binds PEBP2/CBF (AML1)." Molecular and Cellular Biology 14, no. 12 (December 1994): 8085–95. http://dx.doi.org/10.1128/mcb.14.12.8085.

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The receptor for the macrophage colony-stimulating factor (or colony-stimulating factor 1 [CSF-1]) is expressed from different promoters in monocytic cells and placental trophoblasts. We have demonstrated that the monocyte-specific expression of the CSF-1 receptor is regulated at the level of transcription by a tissue-specific promoter whose activity is stimulated by the monocyte/B-cell-specific transcription factor PU.1 (D.-E. Zhang, C.J. Hetherington, H.-M. Chen, and D.G. Tenen, Mol. Cell. Biol. 14:373-381, 1994). Here we report that the tissue specificity of this promoter is also mediated by sequences in a region II (bp -88 to -59), which lies 10 bp upstream from the PU.1-binding site. When analyzed by DNase footprinting, region II was protected preferentially in monocytic cells. Electrophoretic mobility shift assays confirmed that region II interacts specifically with nuclear proteins from monocytic cells. Two gel shift complexes (Mono A and Mono B) were formed with separate sequence elements within this region. Competition and supershift experiments indicate that Mono B contains a member of the polyomavirus enhancer-binding protein 2/core-binding factor (PEBP2/CBF) family, which includes the AML1 gene product, while Mono A is a distinct complex preferentially expressed in monocytic cells. Promoter constructs with mutations in these sequence elements were no longer expressed specifically in monocytes. Furthermore, multimerized region II sequence elements enhanced the activity of a heterologous thymidine kinase promoter in monocytic cells but not other cell types tested. These results indicate that the monocyte/B-cell-specific transcription factor PU.1 and the Mono A and Mono B protein complexes act in concert to regulate monocyte-specific transcription of the CSF-1 receptor.
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Seet, Christopher, Runfeng Miao, Chee Jia Chin, Chong Bin He, Yuhua Zhu, Rebecca Chan, and Gay Crooks. "Identification of a human clonogenic monocyte/macrophage progenitor in fetal and adult hematopoiesis (HEM5P.232)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 120.12. http://dx.doi.org/10.4049/jimmunol.194.supp.120.12.

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Abstract During steady-state hematopoiesis, the monocytic lineage, which includes macrophages, osteoclasts, monocytes, and monocyte-derived dendritic cells (moDCs), arises from a progenitor hierarchy in bone marrow. In humans, multipotent myeloid progenitors such as the granulocyte-monocyte progenitor (GMP) are proximal in this hierarchy, however the distal stages of monocytopoieis are unclear. We report here identification of a human clonogenic, monocytic-committed progenitor with a lineage negative, CD34+ CD38+ CD45RA+ CD123int CD115+ phenotype, which was developmentally conserved across bone marrow, cord blood, and fetal liver. Ex vivo analysis demonstrated a high cloning efficiency, and monocytic but not granulocytic CFU potential. Differentiation in the presence of M-CSF resulted in exclusive production of functional M2-like macrophages, whereas cultures modified with RANKL and GM-CSF/IL-4 resulted in highly enriched cultures of functional osteoclasts and moDCs, respectively. Transplantation into immunodeficient mice reconstituted bone marrow, splenic, pulmonary, and hepatic macrophage subsets, as well as circulating CD14+ monocytic cells. Of note, GMP depleted of CD115+ cells could regenerate the monocytic progenitor phenotype in vitro and in vivo, consistent with a step-wise program of lineage restriction during monocytopoiesis. Identification of the steady-state human monocytic progenitor offers opportunities for therapeutic expansion or modification of the monocytic lineage.
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Полянин, Andrey Polyanin, Поповичева, and Natalya Popovicheva. "PROBLEMS OF DEVELOPMENT OF MONOCITIES IN THE MODERN WORLD." Central Russian Journal of Social Sciences 10, no. 4 (June 30, 2015): 186–93. http://dx.doi.org/10.12737/11965.

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The article deals with the specifics of monocities in Russia, determined by the features of their appearance, funding and degree of stagnation. The authors prove the need for the development of Russian monocities through diversification of their economies, creating new jobs and attracting investments. However, diversification is not the only possible way of development of monocity; it is revealed on the basis of the study, in which the models of development of monocities are considered. One of the problems is specified, non-ability of a number of monocities to diversify, which leads to the opposite effect: increasing the risk of loss of viability of the city. This situation requires further development of an integrated comprehensive approach to the problems of monocities, taking into account the entire spectrum of development features of each city.
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NIKONOVA, Mariya A., and Ekaterina V. AKINFEEVA. "Assessing the demographic situation in single-industry cities: The Nizhny Novgorod agglomeration case study." Regional Economics: Theory and Practice 19, no. 5 (May 14, 2021): 857–79. http://dx.doi.org/10.24891/re.19.5.857.

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Subject. This article deals with the issues of development of the economy of monocities and creation of agglomerations. Objectives. The article aims to assess the impact of an urban agglomeration on changing the demographic situation in the monocities that make up its membership. Methods. Examining the data of the Federal State Statistics Service, and official websites of the Nizhny Novgorod Oblast and monocities under consideration, we used a comparative analysis. Results. Manufacturing and agriculture are the basis of the industry specialization of the monocities under consideration. During the period 2018–2020, the demographic situation in the monocities of the Nizhny Novgorod metropolitan area has not changed much. Conclusions. To include a monocity in the metropolitan area, its various features should be considered. Comprehensive institutional measures to create effective governance models are necessary to heighten an agglomeration effect.
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Dissertations / Theses on the topic "Monociti"

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CORINTI, SILVIA. "Ruolo dell’ossido nitrico sulle funzioni delle cellule dendritiche derivate dai monociti." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2006. http://hdl.handle.net/2108/222.

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L’ossido nitrico (NO) ha un ruolo stabilito nella difesa contro le infezioni batteriche e esercita molteplici attività modulatorie sia sulle risposte infiammatorie che immunologiche. Comunque, la rilevanza di NO sulle funzione delle cellule dendritiche (CD) è stata poco investigata. In questo studio, abbiamo trovato che l’aggiunta di un donatore di NO, S-nitrosoglutathione (GSNO), a CD derivate da monociti maturate con lipopolisaccaride (LPS) o con il ligando solubile di CD40 è legata ad una diminuita capacità di attivare cellule T allogeniche vergini ma con una più prominente polarizzazione di tipo Th1, con un’aumentata secrezione di interferon- (IFN-) e un rilascio ridotto di interleuchina (IL-)5. La presenza di GSNO durante la maturazione delle CD causa una ridotta espressione di superficie di CD86, mentre l’espressione di CD80, di CD83 e delle molecole MHC rimane inalterata. In più, GSNO induce una diminuizione dipendente dalla dose di IL-10 ed aumenta il rilascio di fattore  della necrosi dei tumori (TNF-) da parte di CD mature. In parallelo, si osserva una marcata riduzione di produzione della subunità p40 di IL-12 ma una non significativa perturbazione della produzione della forma bioattiva di IL-12 p70. Infine, GSNO riduce significativamente il rilascio di IP-10/CXCL10 e RANTES/CCL5 ma no di IL-8/CXCL8 da parte delle CD mature. Malgrado GSNO possa rafforzare la capacità delle CD mature di indurre polarizzazione di tipo Th1 dei linfociti T, i nostri dati suggeriscono che induce diverse funzioni anti-infiammatorie, eventualmente riducendo la proliferazione ed il reclutamento dei linfociti T.
Nitric oxide (NO) has an established role in the defense against bacterial infections, and exerts multiple modulatory activities on both inflammatory and immune responses. However, the relevance of NO on dendritic cell (DC) functions has been poorly investigated. In this study, we found that addition of the NO donor S-nitrosoglutathione (GSNO) to monocyte-derived DCs matured in the presence of LPS led to a decreased capacity to activate naive allogeneic T cells but a more prominent Th1 polarization, with increased IFN- secretion and reduced IL-4 and IL-5 secretion. The presence of GSNO during maturation of DCs caused a reduced expression of surface CD86, whereas CD80, CD83 and MHC molecule expression was not affected. Moreover, GSNO induced a dose-dependent decrease of IL-10 and enhancement of TNF- release. In parallel, a marked reduction of IL-12 p40 subunit in the supernatant of mature DCs, but no significant perturbation of the bioactive IL-12 p70 production was observed. Finally, GSNO significantly reduced the release of IP-10/CXCL10 and RANTES/CCL5, but not IL-8/CXCL8 by DCs. Although GSNO can strengthen the capacity of mature DCs to induce type 1 polarization of T lymphocytes, our data suggest that it elicits distinct anti-inflammatory functions, eventually reducing T lymphocyte proliferation and recruitment.
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ANGIULLI, FEDERICA. "NEUROINFLAMMATION IN THE PATHOGENESIS OF ALZHEIMER’S DISEASE: A CENTRAL ROLE FOR PERIPHERAL MONOCYTES." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2022. http://hdl.handle.net/10281/374737.

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La neuroinfiammazione, processo chiave nella malattia di Alzheimer (AD), è mediata da cellule gliali residenti e monociti periferici reclutati a livello centrale. Tuttavia, il ruolo dei monociti nell'AD rimane controverso. Di conseguenza, lo scopo di questo lavoro è quello di studiare il reclutamento dei monociti e capire il loro coinvolgimento nella fagocitosi della β amiloide (Aβ). Particolare attenzione è stata posta al ruolo dei recettori CCR2 e TSPO nella chemiotassi e quello di TREM2 e della sua forma solubile (sTREM2) nella fagocitosi. Inoltre, è stata valutata la capacità di Donepezil, Co-ultraPEALut e anticorpi monoclonali anti-Aβ di influenzare questi processi. Infine, è stato visto il ruolo della neuroifiammazione e del sistema DBI/TSPO nel cluster agitazione/aggressività (A/A) nei disturbi comportamentali associati ad AD (BPSD). Sono stati eseguiti saggi di chemiotassi con camere di Boyden e di fagocitosi mediante microscopia a fluorescenza su linee cellulari e monociti/macrofagi di pazienti AD e controllo. L'Aβ42 oligomerica è stata usata come stimolo chemoattraente e substrato per la fagocitosi; i saggi sono stati condotti anche previa stimolazione con Donepezil, Co-ultraPEALut e anticorpi anti-Aβ (a livelli patologici ridotti). L'espressione di CCR2, TSPO e TREM2 è stata valutata tramite Real-time PCR e Western Blot. I livelli plasmatici di sTREM2 sono stati misurati tramite ELISA, così come i livelli di DBI nel siero e liquor di pazienti A/A. L'espressione di TSPO nei linfomonociti di pazienti A/A è stata valutata tramite Real-time PCR e Western Blot. La migrazione dei monociti di pazienti A/A è stata quantificata con le camere di Boyden. L'Aβ42 promuove la migrazione dei monociti, ma non è in grado di modulare l'espressione di CCR2 e TSPO. I monociti di pazienti AD hanno una ridotta espressione di TREM2, che suggerisce una limitata capacità fagocitica. Il Donepezil inibisce la migrazione Aβ-indotta, e influenza la fagocitosi in linee cellulari e macrofagi umani da soggetti controllo; tuttavia, non ha effetto sui macrofagi dei pazienti AD. Co-ultraPEALut previene la chemiotassi Aβ-indotta e aumenta l'espressione di TREM2 nei macrofagi, probabilmente ristabilendo la loro capacità fagocitica. Gli anticorpi anti-Aβ riducono la chemiotassi Aβ-indotta ma non favoriscono la fagocitosi. I livelli di DBI e l'espressione di TSPO non aumentano nei pazienti A/A, i cui monociti non mostrano neanche alcuna alterazione in termini di attività chemotattica. Nel complesso, questi risultati suggeriscono un coinvolgimento di Aβ42 nella chemiotassi monocitaria nell'AD e la presenza di una ridotta attività fagocitica nei macrofagi dei pazienti AD. I risultati non chiariscono completamente i meccanismi coinvolti nella chemiotassi Aβ-indotta, nonostante puntino chiaramente verso un coinvolgimento del recettore TSPO. Donepezil e Co-ultraPEALut sono emersi come agenti terapeutici validi per contrastare la neuroinfiammazione attraverso la modulazione di chemiotassi e fagocitosi, anche se il loro effetto sui pazienti AD necessita di ulteriori approfondimenti. D'altro canto, per quanto i livelli patologici di anticorpi anti-Aβ siano sufficienti a interferire con il reclutamento dei monociti, è necessario aumentare il loro livello cerebrale per avere un effetto protettivo in termini di fagocitosi dell'Aβ. Infine, i dati suggeriscono che il sistema DBI/TSPO potrebbe non essere coinvolto nella patogenesi del fenotipo agitazione/aggressività dei BPSD. In futuro ci proponiamo di approfondire il ruolo dei recettori coinvolti nella chemiotassi e di completare la caratterizzazione del fenotipo fagocitico dei macrofagi periferici. Studi successivi serviranno anche a validare l'uso terapeutico dei composti testati. Infine, saranno necessari ulteriori esperimenti per comprendere se la neuroinfiammazione può giocare un ruolo nella patogenesi di altri tipi di BPSD.
Background and Aims: Neuroinflammation is a key event in Alzheimer’s disease (AD) and is sustained by resident glial cells and blood derived monocytes attracted into the brain. Still, monocytes contribution to AD is controversial. Therefore, the aim of this study is to investigate monocytes recruitment in the AD brain and to understand their involvement in Aβ clearance. The contribution of CCR2 and TSPO receptors to the regulation of chemotaxis was assessed, toghether with that of TREM2 and its soluble form (sTREM2) to phagocytosis. Moreover, the disease-modifying potential of Donepezil, Co-ultraPEALut and anti-Aβ monoclonal antibodies (mAb) - in relation to their ability to influence these processes - was evaluated. Finally, the potential implication of neuroinflammation and the DBI/TSPO system in the agitation/aggression (A/A) cluster of Behavioral and Psychological Symptoms of Dementia (BPSD) was assessed. Materials and Methods: Boyden chamber chemotaxis assays and fluorescence microscopy-based phagocytosis assays were performed on monocytic cell lines and monocytes/macrophages from AD patients and controls. Oligomeric Aβ42 was used as chemoattractant and phagocytic target; the assays were also performed upon stimulation with Donepezil, Co-ultraPEALut and anti-Aβ mAb (at pathologically low levels). Expression of CCR2, TSPO and TREM2 were investigated through Real-time PCR and Western Blot analysis; plasma levels of sTREM2 were measured by ELISA. DBI levels were assessed by ELISA in CSF and serum of A/A patients. TSPO expression in lymphomonocytes from A/A patients was determined by Real-time PCR and Western Blot. Migration of monocytes from A/A patients was quantified through Boyden chamber assay. Results: Aβ42 promotes monocytes migration, but is not able to modulate CCR2 and TSPO expression. Monocytes from AD patients have reduced TREM2 expression, suggestive of limited phagocytic activity. Donepezil inhibits Aβ-induced migration, and impacts the phagocytic activity of cell lines and human macrophages from healthy controls; however, it fails to show any effect in macrophages from AD patients. Co-ultraPEALut prevents Aβ-induced chemotaxis and increases TREM2 expression in macrophages, probably recovering their phagocytic competence. Anti-Aβ mAb decrease Aβ-induced migration, but are not able to increase phagocytosis. DBI levels and TSPO expression do not increase in A/A patients, and monocytes from A/A patients do not show any difference in terms of chemotactic activity compared to their counterparts. Discussion: Taken together, these findings suggest an involvement of Aβ42 in the chemotaxis of monocytes in AD and a reduced phagocytic activity charachterizing macrophages from AD patients. The results fail to completely elucidate the mechanisms underlying Aβ-induced migration, even though they clearly point towards an involvement of TSPO in the process. Donepezil and Co-ultraPEALut emerge as useful therapeutic agents with the potential to counteract neuroinflammation by modulating chemotaxis and phagocytosis, despite treatment response in AD patients requiring additional investigations. On the other hand, an increase in specific anti-Aβ mAb in the brain of AD patient is required to deliver a protective effect in terms of plaque clearance, despite pathologically low intrathecal levels being already sufficient to interfere with monocyte recruitment. Finally, data suggest that the DBI/TSPO system may not be involved in A/A pathogenesis. Conclusion: In the future we propose to elaborate on the modulation of receptors involved in chemotaxis and to complete the characterization of the phagocytic phenotype of peripherally-derived macrophages. Future studies will be also aimed at validating the therapeutic use of the selected disease-modifying compounds. Finally, more experiments will be necessary to understand if neuroinflammation could play a role in the pathogenesis of other BPSD clusters.
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GAUDIO, ANNAMARIA. "Effetti in vivo e in vitro della vitamina D nell'artrite reumatoide." Doctoral thesis, Università di Foggia, 2015. http://hdl.handle.net/11369/338379.

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Abstract L’1,25-diidrossivitamina D (1,25 (OH) 2D3), la forma attiva della vitamina D, modula entrambe le risposte immunitarie: innata e adattativa. Emergenti dati epidemiologici hanno anche dimostrato che la vitamina D ha effetti immunomodulatori e modificanti la malattia in una vasta gamma di malattie autoimmuni, tra cui l'artrite reumatoide (AR). Lo studio in vivo ha mostrato la correlazione tra i livelli sierici della 25OH vitamina D e l'attività della malattia e lo stato di salute di pazienti con AR mediante la valutazione del DAS 28 e HAQ. L'analisi statistica non solo ha dimostrato una correlazione tra l'attività della malattia e i livelli di 25 OH vitamina D, ma anche una correlazione negativa tra i valori di 25OH vitamina D e DAS 28 e HAQ. I livelli di 25 OH vitamina D in pazienti con AR erano significativamente inferiori a quelli del gruppo di controllo. In vitro è stato valutato l’effetto della 1,25 (OH) 2D3 in colture primarie di macrofagi di pazienti AR derivati dai monociti del sangue periferico. I monociti/ macrofagi, isolati da sangue periferico di cellule mononucleate di pazienti AR e di soggetti sani sfruttando la loro capacità di aderire alla piastra, sono stati trattati con concentrazioni crescenti di 1,25 (OH)2D3 per 48 h. La produzione di TNF-α, IL-1 α, IL-1β, IL-6 e RANKL è stata determinata mediante ELISA ed il rilascio di ossido nitrico (NO) mediante il metodo GRIESS. L’analisi immunocitochimica è stata effettuata anche per valutare le alterazioni nell’espressione del TNF-α transmembrana dopo trattamento con 1,25 (OH) 2D3. È stata osservata una significativa diminuzione dose-dipendente della produzione di TNF-α e RANKL nelle colture di macrofagi AR dopo trattamento, mentre nelle cellule sane solo ad alte concentrazioni di trattamento con 1,25 (OH) 2D3. I livelli di IL-1 α, IL-1β e IL-6 sono stati ridotti in tutte le popolazioni cellulari ad alte concentrazioni. L’immunoistochimica del TNF- α è risultata meno intensa nelle cellule trattate rispetto a quelle non. L’1,25 (OH) 2D3 ha ridotto in modo significativo i livelli di ossido nitrico (NO) a prescindere dalle concentrazioni utilizzate. Tutti questi effetti osservati forniscono un razionale terapeutico nell’utilizzare la supplementazione della vitamina D nel trattamento dell’AR. Abstract 1,25-Dihydroxyvitamin D (1,25(OH)2D3), the active form of vitamin D, modulates both innate and adaptive immune responses. Emerging epidemiological data have also demonstrated disease-modifying and immunomodulatory effects of vitamin D in a wide range of human autoimmune diseases, including rheumatoid arthritis (RA). DAS 28 and HAQ were evaluated in order to evaluate in vivo the relationship between serum 25 OH vitamin D levels and disease activity and health status in RA. Statistical analysis showed not only a correlation between disease activity and the levels of 25 OH vitamin D, but also a negative correlation between the values of 25OH vitamin D and DAS 28 and HAQ. The levels of 25 OH vitamin D in RA patients were significantly lower than in the control group. To evaluate in vitro effects of 1,25(OH) 2D3 in primary cultures of peripheral blood monocyte-derived macrophages of RA patients, monocytes/macrophages, isolated from peripheral blood mononuclear cells of RA patients and healthy subjects by exploiting their ability to adhere to plastic, were treated with increasing concentrations of 1,25(OH)2D3 for 48 h. TNF-α, IL-1 α, IL-1β, IL-6 and RANKL production was determined by ELISA and nitric oxide (NO) release using the Griess method. Immunocytochemistry analysis was also performed to evaluate alterations in transmembrane TNF- α expression after 1,25(OH) 2D3 treatment. A significant dose-dependent decrease in TNF- α and RANKL production by cultured RA macrophages after 1,25(OH)2D3 treatment was found, whereas a significant reduction in normal cells was observed only at higher concentrations. IL-1 α, IL-1β and IL-6 levels were reduced by 1,25(OH) 2D3 at higher concentrations in all cell populations. TNF-a immunostaining was less intense in treated cells compared with untreated. 1,25(OH) 2D3 significantly reduced NO levels regardless of the concentration used. Vitamin D downregulated proinflammatory mediators in monocyte-derived macrophages, and RA cells appeared more sensitive than normal cells. These effects further provide a rationale for the therapeutic value of vitamin D supplementation in the treatment for RA.
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Cappellari, Roberta. "The monocyte continuum and cardiovascular disease: Evaluation of the prognostic cardiovascular meaning of monocyte displacement along their continuum." Doctoral thesis, Università degli studi di Padova, 2018. http://hdl.handle.net/11577/3425891.

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Introduction. Monocytes are cells of the innate immunity system with high heterogeneity and plasticity and are involved in acute and chronic inflammatory states. Monocytes are traditionally distinguished in three subsets, based on CD14 (LPS co-receptor) and CD16 (FcγIII receptor with low IgG affinity) expression: classical, intermediate and non-classical. Monocyte subsets have a developmental relationship and differ in phenotypic and functional characteristics. Distribution of monocyte subsets has been shown to predict cardiovascular outcomes. Nevertheless, monocytes have now been redefined as a continuum of subsets with dynamic changes of their characteristics and classification into different subtypes may be an oversimplification. Monocytes have been studied in cardiovascular diseases because they are involved in inflammatory processes linked with these pathological states: they have a central role in the development of atherosclerotic plaques, that represent the major cause of cardiovascular events. Changes within different monocyte subsets are reported in several studies in relation with cardiovascular risk factors and cardiovascular diseases. Aim of the study. The aim of this study is to establish whether distribution of monocytes based on CD14 and CD16 fluorescence intensity provides incremental and complementary information in relation to cardiovascular risk factors, prevalent cardiovascular diseases and cardiovascular outcomes beyond enumeration of traditional subsets. Materials and methods. A cohort of 227 patients with high cardiovascular risk (patients with at least two classical cardiovascular risk factors or with establish cardiovascular disease) were recruited for this study and followed up for a median of 4 years. Monocyte subsets were quantified and characterized at baseline using polychromatic flow cytometry, based on the CD14 e CD16 expression; for each monocyte subset frequency and mean fluorescence intensity (MFI) of CD14 and CD16 were determined, evaluating the continuous distribution. These monocyte characteristics were studied in patients in relation to cardiovascular risk factors, prevalence of coronary artery disease (CAD) and occurrence of major adverse cardiovascular events (MACE) during follow-up. Results. In relation to cardiovascular risk factors, every monocyte subset of patients with type 2 diabetes showed a consistent shift toward higher CD16 fluorescence intensity, despite no changes in their frequencies. Patients with coronary artery disease (CAD) at baseline displayed a doubled amount of CD14++ CD16+, intermediate monocytes, and a shift of non-classical and classical monocytes towards intermediates ones. During follow-up, cardiovascular death or cardiovascular events occurred in 26 patients, who showed monocyte displacement similar to those of patients with CAD at baseline. Using a Cox proportional hazard regression models, among monocytes parameters, only the higher CD16 expression on classical monocytes, independently predicted adverse cardiovascular outcomes, but not the level of intermediate monocytes or other subsets. Discussion and conclusion. Changes within monocyte subsets in patients with CAD and in patients with incident MACE during follow-up suggested a shift of classical and non-classical monocytes towards intermediate monocytes, showing phenotypic changes within the monocyte continuum. The predictive role of CD16 MFI on classical monocytes highlights how the concept of monocyte continuum can be used to shape the cardiovascular risk more than frequencies of monocyte subsets can do.
Introduzione. I monociti sono cellule del sistema dell’immunità innata con elevata eterogeneità e plasticità e sono coinvolti in stati infiammatori acuti e cronici. I monociti sono tradizionalmente distinti in tre sottopopolazioni, in base all'espressione del CD14 (co-recettore dell’LPS) e CD16 (recettore FcγIII con bassa affinità per IgG): classici, intermedi e non classici. Questi sottogruppi monocitari hanno una relazione evolutiva e differiscono per caratteristiche fenotipiche e funzionali. La distribuzione dei sottoinsiemi monocitari ha dimostrato di prevedere gli esiti cardiovascolari. Tuttavia, i monociti sono recentemente stati ridefiniti come un continuum di sottoinsiemi con cambiamenti dinamici delle loro caratteristiche e la categorizzazione in sottoinsiemi discreti può essere considerata come un’eccessiva semplificazione. Nelle malattie cardiovascolari i monociti sono stati studiati in quanto coinvolti in processi infiammatori legati a questi stati patologici: hanno un ruolo centrale nello sviluppo delle placche aterosclerotiche, che rappresentano la principale causa per gli eventi cardiovascolari. Diversi studi hanno dimostrato cambiamenti all'interno dei sottoinsiemi monocitari in relazione ai tradizionali fattori di rischio cardiovascolare e alle patologie cardiovascolari. Scopo dello studio. Lo scopo di questo studio è stabilire se la distribuzione dei monociti basata sull'intensità di fluorescenza del CD14 e del CD16 fornisce informazioni incrementali e complementari in relazione ai fattori di rischio cardiovascolare, alle patologie cardiovascolari prevalenti e agli esiti cardiovascolari rispetto alla quantificazione della frequenza dei sottogruppi tradizionali. L'obiettivo dello studio è anche quello di verificare se questi cambiamenti predicono esiti cardiovascolari. Materiali e metodi. 227 pazienti ad alto rischio cardiovascolare (pazienti con almeno due classici fattori di rischio cardiovascolare o con malattia cardiovascolare stabilita) sono stati reclutati per questo studio e seguiti per una mediana di 4 anni. Le sottopopolazioni monocitarie sono state quantificate e caratterizzate al basale utilizzando la citometria a flusso policromatica, in base all'espressione di CD14 e CD16; per ciascun sottogruppo sono stati determinati la frequenza e l’ intensità media di fluorescenza (MFI) di CD14 e CD16, valutando la loro distribuzione lungo il continuum monocitario. Queste caratteristiche dei monociti sono state studiate nei pazienti correlandole ai fattori di rischio cardiovascolare, alla prevalenza di malattia coronarica (CAD) e alla comparsa di eventi avversi cardiovascolari maggiori (MACE) durante il follow-up. Risultati. In relazione ai fattori di rischio cardiovascolare, nei pazienti con diabete di tipo 2 è stato osservato un aumento consistente dell’ intensità di fluorescenza del CD16 all'interno di ciascun gruppo di monociti, nonostante non si sia rilevato nessun cambiamento nelle loro frequenze. I pazienti con malattia coronarica (CAD) al basale hanno mostrato un raddoppio nella frequenza dei monociti intermedi CD14++ CD16+ e uno spostamento di monociti classici e non classici verso quelli intermedi. Durante il follow-up, la morte cardiovascolare o eventi cardiovascolari si sono verificati in 26 pazienti, che hanno mostrato uno spostamento dei monociti simile a quelli dei pazienti con CAD al basale. Utilizzando il modello di Cox di regressione di rischio proporzionale, tra i parametri dei monociti, solo l'espressione del CD16, più elevata sui monociti classici, ma non il livello di monociti intermedi o di altri sottogruppi, predice indipendentemente gli eventi cardiovascolari avversi. Discussione e conclusione. I cambiamenti nei sottogruppi monocitari in pazienti con CAD e in pazienti evoluti in MACE durante il follow-up hanno suggerito uno “shift” dei monociti classici e non classici verso gli intermedi, mostrando cambiamenti fenotipici all'interno del continuum monocitario. Il ruolo predittivo dell’MFI del CD16 sui monociti classici evidenzia come il concetto di continuum monocitario possa essere utilizzato per modellare il rischio cardiovascolare più della frequenza delle diverse sottopopolazioni monocitarie.
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Curtarello, Matteo. "Valutazione dell'effetto immunomodulatorio della Glicoproteina vOX2 dell'Herpesvirus umano di tipo 8 su monociti-macrofagi." Doctoral thesis, Università degli studi di Padova, 2008. http://hdl.handle.net/11577/3426380.

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Aim of this work is to clarify the human herpervirus 8 vOX2 activity in monocytes-macrophages in order to define its funtional role in Kaposi Sarcoma pathogenesis. Kaposi’s Sarcoma (KS) is an inflammatory cytokines-mediated angioproliferative disease triggered by human herpesvirus 8 (HHV-8) infection. This virus is unique because of its extensive molecular piracy of host critical cell regulatory and immune modulatory genes encoding proteins that could contribute to viral immune evasion and tumorigenesis. Among them we can find the vOX2 glycoprotein. Cellular homologous OX2 is a member of the immunoglobulin superfamily. This glycoprotein is expressed by several cell types in vivo and it down-modulates inflammatory response through the interaction with a specific receptor of the myeloid cells, the CD200R. By this mechanism, cellular OX2 prevents autoimmune disease, displaying immune modulatory functions. This latter feature is also present in the HHV-8 vOX2. Indeed, several reports suggest that the vOX2 has an anti-inflammatory and immunosuppressive activity in basophil and neutrophil cells, but its effect on monocytes-macrophages is still controversial. The aim of our work is to clarify the vOX2 activity in monocytes-macrophages in order to define its functional role in KS pathogenesis. The relevance of monocytesmacrophages relies on the fact that this cell type is infected by HHV-8 in vivo, it is present in KS lesions and it expresses CD200R that functions as a receptor for vOX2 exactly like it does for cellular OX2. We decided to express the viral glycoprotein into two different monocyticmacrophagic cell lines (U937 and THP1) and/or into PBMC-derived macrophages (primary MØ) for our study. Compared to chemical and physical methods, the viral transduction has resulted the most efficient system to transfer transgenes into the target cells; based on this finding, the HHV-8 orf K14 encoding vOX2 has been cloned into HIV-1 based lentiviral vector that has been used to transduce the cells. After verifying the vOX2 expression in the transduced target cells, we evaluated the glycoprotein effect on the transcription level and secretion of two inflammatory cytokines involved in the KS development, TNF? and IL-1?. Our data show that the vOX2 up-regulates both TNF? and IL-1? in U937 and THP1 cell lines and in primary MØ kept in basal conditions. In addition, the TNF? and IL-1? up-regulation was observed in the IFN?-activated U937 cell line. By contrast, in the IFN?-activated THP1 cell line and primary MØ the viral glycoprotein inhibits TNF? and IL-1? gene expression. Taking into account these controversial data in the different cell types, in order to carry on our research in a model more representative of the physiological condition, we checked the expression of vOX2 receptor on U937 and THP1 cell line and on primary MØ. Since the primary MØ resulted to be the only cell type expressing CD200R, we decided to evaluate the vOX2 activity employing this cellular system. However, being the level of viral protein expression in primary MØ low compared to the one obtained in the cell lines, we performed coculture between THP1 CD200R¯ cell line expressing vOX2 and primary MØ CD200R+ in order to confirm the results on inflammatory-cytokines modulation by vOX2. Our data show that the vOX2 promotes TNF? secretion in the primary MØ in basal conditions; on the contrary, in the IFN?-activated cells the viral glycoprotein induces a significant reduction of cytokine production as we observed in monoculture of primary MØ expressing vOX2. Starting from these data, we next evaluated the vOX2 effect on the transcription level of IL-10, an inhibitory cytokine of the TNF? and IL-1?-mediated inflammatory responses. Our data show that IL-10 expression profile is the opposite with respect to TNF? and IL-1?, as we expected. Moreover, these results are in agreement with the CD200R mRNA down-modulation that we observed in basal conditions and with its up-regulation in the IFN?-activated cells. In addition, we were able to show that vOX2 promotes the phagocytosis of the primary MØ in basal conditions while it inhibits this activity in the IFN?-activated cells. Our results suggest that the immune modulatory activity of vOX2 is tightly dependent on the activation state of the cells. This conclusion is also supported by the analysis of vOX2 effect on the global gene expression profile in the primary MØ. Finally, we observed that the antigen presentation to T cells by primary MØ is compromised by vOX2 expression regardless of the activation state of the cells. This effect seems to be related to the down-modulation of HLA expression on cell surface. Overall, our results lead to the conclusion that vOX2 may be involved in viral immune evasion because of its anti-inflammatory and immunosuppressive effect in the activated monocytes-macrophages. At the same time, in basal conditions, vOX2 can also stimulate monocytes-macrophages contributing to the inflammatory state that is important for the KS development. This finding would imply the presence of at least one unknown receptor that would compete with the “inhibitory receptor” CD200R for the binding to vOX2. An immune modulatory activity of vOX2, linked to cell activation state, could explain the contradictory results reported in literature.
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Cecchini, Paola. "NadA da Neisseria meningitidis interagisce con Hsp90 sulla superficie dei monociti modulando la loro produzione di citochine." Doctoral thesis, Università degli studi di Padova, 2008. http://hdl.handle.net/11577/3425195.

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Neisseria meningitidis is an encapsulated, Gram-negative bacterium that colonizes the upper respiratory tract of ~10% of humans. With a frequency of one to three cases per 100.000 of the population, the bacterium enters the bloodstream, where it multiplies to high density and cause sepsis. From the bloodstream the bacterium can cross the blood-brain barrier and cause meningitis. The invasive infection is very dramatic, affecting mostly infants, children, and adolescents who do not have bactericidal antibodies against the infecting strains. Immunity against the disease can be acquired naturally or induced by vaccination and correlates with the presence of antibodies able to kill the bacterium in the presence of complement. There are no effective vaccines currently licensed in the Unit States or Europe for prevention of the disease caused by serogroup B meningococcus. The genome sequencing of Neisseria meningitidis, serogroup B, allowed the identification of unknown surface proteins termed GNA (Genome derived Neisseria Antigens) among which NadA (Neisseria Adhesin A). NadA is a highly conserved protein among disease-associated strains and capable of eliciting bactericidal antibodies in mice. Structure prediction and homology comparison with know virulence-associated factors suggest that NadA belongs to the group of OCA (Oligomeric Coiled-coil Adhesin) nonfimbrial adhesins. Recently, NadA has been characterized as a new meningococcic factor, involved in the colonization and the invasion of host cells. Probably there is a unique receptor expressed in different cellular lines. In this thesis, we have focused on unravelling the identity of this possible receptor for NadA in these cells. To identify the specific receptor for NadA, experiments of co-immunoprecipitation and overlay were performed in Chang total cell lysates. Our data suggest as possible receptor a protein of 90 kDa, that was present in the co-immunoprecipitation samples incubated with NadA and absent in controls. Subsequently, this protein obtained by co-immunoprecipitation of NadA, was enriched, separated by 12% SDS-PAGE, then excised from the gel and subjected to tryptic proteolysis; resulting peptides were analyzed by liquid chromatography/MS and data were analyzed with the Mascot software. In this way, we identified the human Heat shock protein 90\beta, as the recognized peptides provide a coverage of 25% of the total protein sequence . To confirm the MS data, co-immunoprecipitation samples and membrane proteins from Chang cells were incubated with antibody anti-Hsp90, in order to demonstrate a membrane localization of Hsp90, which is generally known as a cytoplasmic protein. However, as described in the literature, Hsp90 can be expressed on the surface of various cell types, such as tumor and apoptotic cells, but also on HeLa cells, monocytes, macrophages and dendritic cells. Our results confirm that Hsp90 is also found in the cell membrane of Chang cells. Moreover, we found that in co-immunoprecipitation experiments addition of polymyxin B, a cationic antibiotic similar to antimicrobic peptides produced by monocytes that binds both to NadA and Hsp90, is able to interfere in the interaction of NadA with Hsp90. In order to investigate the effect of the association between NadA and Hsp90 in cells, we quantified the superficial expression of Hsp90 on Chang cells and on human monocytes, isolates from Buffy coat , which were found to be 2% and 5% of total cell surface protein, respectively Since the mechanism of transport to the plasma membrane remains enigmatic, we quantified the superficial expression of Hsp90 in Chang cells after the incubation with rHsp90, but we didn’t see an increase of protein expression. We also performed experiments on human monocytes, which are the main agonist of the innate immune system, in order to study the receptorial function of this association, and also the involvement of the immune system. Monocytes were incubated with antibodies anti-Hsp90, with or without Polymyxin B, and then they were analyzed by FACS, to quantify the binding of NadA-alexa. These experiments showed that the NadA binding to the cells is not influenced by the presence of the anti-Hsp90 antibody. We also investigated whether the superficial expression of Hsp90 in monocytes changed after pre-incubation with NadA. By FACS analysis, we quantified the fluorescence of a PE conjugated secondary antibody after the incubation with anti-Hsp90 antibodies. The results showed that pre-incubation with NadA interferes with the recognition of the superficial Hsp90 by its specific antibodies, showing a decrease of 40%, which could be explained by the competive association between NadA and Hsp90 on the plasmatic membrane. Moreover, when monocytes were incubated with NadA for 3h at 37°C in presence of Polymyxin B, we did not observe decrease on the signal. Taken together, these data indicate that NadA-Hsp90 association is not a receptorial one, indicating that, under physiological conditions, these proteins bind closely and strongly each others, probably producing clusters on the plasma membrane. Finally, to analyze the effect of these complexes on the activation of the immune system, we analyzed the pattern of cytokines produced by human monocytes stimulated for 24h with NadA, antibodies anti-Hsp90 and antibodies anti-TLR2 and 4, and with or without Polymyxin B. These results show a synergic effect of NadA and antibody anti-Hsp90 on cytokines production, mainly IL-6, TNF? and MCP-1; on the contrary, Polymyxin B and antibody anti-TLR4 inhibited cytokines production. The cytokine pattern secreted demonstrated that NadA and Hsp90 induce a macrophage-like phenotype and that these two agonists promote a Th2 response.
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NIKA, Ervin. "VAV1 NEL DIFFERENZIAMENTO MONOCITO/MACROFAGICO DI PRECURSORI MIELOIDI TUMORALI." Doctoral thesis, Università degli studi di Ferrara, 2012. http://hdl.handle.net/11392/2389274.

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Vav1 is a critical signal transducer for the development and function of normal hematopoietic cells, in which it regulates the acquisition of maturation-related properties, including adhesion, motility, and phagocytosis. In addition, Vav1is a key player in the ATRAinduced completion of the differentiation program of tumoral myeloid precursors derived from APL, in which it promotes the acquisition of a mature phenotype by playing multiple functions at both cytoplasmic and nuclear levels. Here we investigate the possible role of Vav1 in the differentiation of leukemic precursors to monocytes/macrophages. Tumoral promyelocytes in which Vav1was negatively modulated were induced to differentiate along the monocytic/macrophagic lineage with ATRA and PMA and monitored for their maturation-related properties. We found that Vav1 is crucial for the phenotypical differentiation of tumoral myeloid precursors to monocytes/macrophages, in terms of CD11b expression, adhesion capability and cell morphology. Confocal analysis revealed that Vav1 may synergize with actin in modulating nuclear morphology of PMA-treated adherent cells. Moreover, Electrophoretic Mobility Shift Assays indicated that Vav1 and the transcription factor PU.1 are recruited to CD11b promoter, suggesting that the two proteins cooperate to regulate the expression of the surface antigen CD11b. The reported results constitute the first evidence thatVav1 plays a crucial role in the maturation of tumoral myeloid precursors to monocytes/macrophages. Since Vav1 is also critical for the maturation of leukemic promyelocytes along the granulocytic lineage, our data highlight the key role for this protein during the completion of the differentiation program of tumoral myeloid cells along the various hematopoietic lineages and suggest that Vav1 is a common target for developing future treatment strategies for the diverse subtypes of myeloid leukemias.
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GRANATA, VALENTINA. "The multitasking role of monocytes in the bone marrow haematopoietic niche: from the drug-resistance to the maintenance of stem cells." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/262915.

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Monociti e macrofagi sono elementi fondamentali all’interno di una nicchia ematopoietica sia fisiologica che patologica. Infatti, tali cellule possono regolare il mantenimento e il differenziamento delle cellule staminali ematopoietiche e contribuire all’aumento della resistenza delle cellule staminali leucemiche in seguito a trattamento chemioterapeutico. Nella prima parte del progetto, abbiamo testato un nuovo regime di condizionamento in un modello murino poco permissivo (Scid-Beige), ricreando un sistema efficace per lo studio dell’ematopoiesi umana fisiologica e patologica. Combinando l’irradiamento con la Fludarabina, un farmaco immunosoppressivo normalmente utilizzato come sistema di condizionamento in clinica, siamo stati in grado di aumentare l’attecchimento delle cellule umane in topi SCID-beige rispetto al medesimo modello murino condizionato con solo irradiamento. Probabilmente, tale effetto è dovuto alla capacità della Fludarabina di ridurre l’attività immunitaria dei linfociti. Attraverso l’utilizzo di questo modello murino, è stato possibile osservare come, la presenza di monociti, possa aumentare notevolmente l’attecchimento delle cellule staminali ematopoietiche. Infatti, i monociti, in vitro, aumentano la sopravvivenza delle cellule CD34+ e permettono il mantenimento della sottopopolazione CD34+CD38-, sia tramite contatto diretto che attraverso il rilascio di fattori solubili. I monociti classici (CD14+CD16-) sembrano essere i principali responsabili di questo effetto: la presenza di monociti classici in co-coltura con CD34+ permette il mantenimento dello stato indifferenziato e garantisce un corretto attecchimento delle cellule staminali umana in topi NSG. Inoltre, sono stati valutati anche possibili meccanismi d’azione (Notch e COX-2/PGE2) che possono essere implicati in tale processo di mantenimento. In aggiunta, nel presente progetto di tesi, è stata ampiamente investigata l’efficacia del farmaco Asparaginasi (ASNase) nel trattamento di leucemie mieloidi acute (LMA) utilizzando materiale da pazienti alla diagnosi. In primo luogo, è stato considerato l’effetto antileucemico di tale farmaco nei blasti LMA e in particolare nella sottopopolazione dei progenitori (CD34+CD38+ CD34+CD38-), dimostrando che sono intrinsecamente suscettibili al farmaco. Successivamente, abbiamo valutato la tossicità di tale farmaco contro le cellule LMA in relazione ad altri componenti cellulari che possono regolare la sensibilità delle cellule staminali leucemiche al trattamento chemioterapico. Tali cellule includono le mesenchimali stromali e i monociti/macrofagi che sembrano produrre rispettivamente asparaginasi (ASNS) e catepsina B (CTSB), quest’ultima in grado di inattivare ASNase, aumentando la resistenza dei blasti a tale trattamento.
Monocytes/macrophages are crucial component of the normal and malignant niche. In fact, they can regulate HSC self-renewal and differentiation and contribute to increase resistance of leukemic cells to chemotherapy. In the first part of the project, we tested the use of a new conditioning regimen in a poor permissive mouse (SCID-beige) to generate an effective xenograft model of human normal and, above all, malignant haematopoiesis. Combining irradiation and Fludarabine, an immunosuppressive drug used in conditioning regimen in clinic, we were able to augment the human engraftment level in SCID-beige mice as compared to irradiation only, probably due to Fludarabine effect on murine leaky lymphocytes. Using this xenograft model, we have observed that when HSC are transplanted in combination with monocytes, there is a massive increment in human haemopoietic engraftment. Moreover, we demonstrated that monocytes increase in vitro CD34+ cell survival and retain CD34+CD38- multipotent stem cells subpopulation, by both contact- and soluble factors-dependent mechanisms. The classical monocyte subset (CD14+CD16-) is primary responsible to maintain HSC survival and prevent their differentiation. In fact, HSC co-cultured with classical monocytes retain their CFC potential and haematopoietic repopulation activity following intravenous injection in NSG mice. Finally, we observed that Notch and COX-2/PGE2 pathways seems to be involved in this crosstalk. In addition, we deeply investigated ASNase effectiveness against AML cells derived from newly diagnosed patients. Firstly, we considered the anti-leukaemic effects on the bulk population and, most importantly, on AML progenitors (clonogenic cells and, especially, CD34+CD38+ CD34+CD38- LSC), showing that they are intrinsically susceptible to ASNase. Secondly, we evaluated the ASNase toxicity against AML in relation with other BM niche cellular components that can regulate the LSC sensitivity to chemotherapy. These cells include mesenchymal stromal cells and monocytes/macrophages that seem to produce respectively ASNS and CTSB, which inactivate ASNase, increasing the resistance to ASNase treatment.
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SAVINETTI, ILENIA. "Specific Signatures in Peripheral Blood Monocytes Stratify Multiple Sclerosis Patients Phenotypes." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2022. http://hdl.handle.net/10281/365445.

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La Sclerosi Multipla (MS) è una patologia autoimmune cronica che colpisce il sistema nervoso centrale (SNC) determinando demielinizzazione. I principali fenotipi patologici sono Recidivante-Remittente (RRMS) e Primariamente Progressiva (PPMS) – quest’ultima è la forme più grave. Ajami B. et al. hanno dimostrato che nel modello murino affetto da Encefalomielite (EAE) - il modello animale di MS- vi è una forte correlazione tra la presenza di monociti a livello del SNC ed il peggioramento dei sintomi motori tipici della malattia. Partendo da queste evidenze , per il nostro studio sono stati prelevati campioni di sangue da HC, RRMS e PPMS -tutte femmine- per poi isolare i monociti CD14+. Su tali campioni sono stati condotti esperimenti microarray e successivamente qRT-PCR. L’analisi bioinformatica ha evidenziato che gli RRMS si distribuivano formando due gruppi: un gruppo (RR1) si distribuiva similmente agli HC, l’altro (RR2) si distribuiva similmente ai PPMS. Dalla Gene Ontology è emerso che i processi biologici maggiormente deregolati erano quelli di Infiammazione e Colesterolo. In aggiunta a questi pazienti, è stata validata tramite qRT-PCR una seconda coorte di RRMS e PPMS. La validazione tramite qRT-PCR ha confermato che i geni coinvolti nella biosintesi del colesterolo sono deregolati nei pazienti di entrambe le coorti, ma con specifiche differenze basate sul paziente. Infatti, sia per gli RRMS che per i PPMS si sono potute apprezzare differenze nei livelli di espressione dello stesso gene anche tra i pazienti con lo stesso fenotipo clinico. Questa deregolazione a livello metabolico, ha permesso di ipotizzare che i monociti di questi pazienti possano avere un fenotipo concordante con la Trained Immunity (TI), recentemente scoperta. Per TI si intende la memoria dell’immunità innata: monociti venuti in contatto con uno stimolo primario conserverebbero memoria di tale “incontro” reagendo in maniera più violenta ad una seconda stimolazione come potrebbe essere uno stimolo infiammatorio. Il primo stimolo può essere indifferentemente un vaccino o molecole come mevalonato (intermedio della biosintesi del colesterolo), β-Glucano e LDL ossidato (oxLDL). Per verificare questa ipotesi abbiamo testato l’espressione di geni che possono essere coinvolti nella TI, tra cui CD36, SR-A, OLR1 – collegati all’oxLDL- NLRP3, DECTIN-1 (codifica per il recettore del β-Glucano) e KDM6B (legato a modificazioni epigenetiche). I più deregolati sono risultati essere OLR1 e DECTIN-1, ma in modo diverso tra le due coorti. In particolare, la coorte 1 risulta più deregolata. Per quanto riguarda il pathway infiammatorio, invece, non è stata osservata la stessa deregolazione nella coorte 1 e nella coorte 2. La coorte 1 è risultata tendenzialmente più infiammata rispetto alla coorte 2, in particolare per i geni TNFα, CXCL2, CXCL3 e CXCL8. A seguito di questi risultati molecolari, si è proceduto con la messa a punto di un possibile modello in vitro. Stimolando ThP1 (monociti umani immortalizzati) con LPC (componente principale dell’oxLDL) si è osservata una corrispondente up-regolazione sia dei geni del colesterolo che dei geni infiammatori (NLRP3, TNFα), confermando di fatto che Infiammazione e Colesterolo viaggiano di pari passo. Per finire, sui pazienti della coorte 1 analizzati con microarray, è stata effettuata l’analisi del miRnoma che ha identificato miRNA collegati ai geni del colesterolo. Alla luce di questi risultati, dove è stato possibile caratterizzare meglio la coorte 1 che la coorte 2, e date le differenze riscontrate anche tra pazienti dello stesso fenotipo clinico di MS, si suggerisce un approccio di tipo personalizzato partendo da una signature molecolare, in modo da definire il profilo di ogni paziente. Inoltre, questo studio suggerisce che per almeno dei sottotipi di pazienti con MS, un trattamento con statine potrebbe essere un importante aiuto nel miglioramento dei sintomi.
Multiple Sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS) leading to demyelination. The main pathological phenotypes are Relapsing-Remitting (RRMS) and Primary Progressive (PPMS) - the latter being the most severe form. Ajami B. et al. have shown that in the mouse model affected by Encephalomyelitis (EAE) - the animal model of MS- there is a strong correlation between the presence of monocytes at the level of the CNS and the worsening of the motor symptoms typical of the disease. Based on this evidence, blood samples from HC, RRMS and PPMS -all female- were collected for our study and CD14+ monocytes were isolated. Microarray experiments were conducted on these samples and subsequently qRT-PCR was performed. Bioinformatics analysis showed that RRMS distributed in two groups: one group (RR1) had similar trend to HC, the other group (RR2) had similar trend to PPMS. Gene Ontology showed that the most deregulated biological processes were those of Inflammation and Cholesterol. In addition to these patients, a second cohort of RRMS and PPMS was validated by qRT-PCR. Validation by qRT-PCR confirmed that the genes involved in cholesterol biosynthesis were deregulated in patients of both cohorts, but with specific patient-based differences. In fact, for both RRMS and PPMS, differences in expression levels of the same gene could be appreciated even among patients with the same clinical phenotype. This deregulation at the metabolic level, allowed us to hypothesize that the monocytes of these patients may have a phenotype consistent with the recently discovered Trained Immunity (TI). By TI is meant the memory of innate immunity: monocytes come into contact with a primary stimulus would retain memory of such "encounter", reacting more violently - and in the case of Multiple Sclerosis in an autoimmune way - to a second stimulation as could be an inflammatory stimulus. The first stimulus may be either a vaccine or molecules such as mevalonate (intermediate cholesterol biosynthesis), β-Glucan, and oxidized LDL (oxLDL). To verify this hypothesis, we tested the expression of genes that may be involved in IT, including CD36, SR-A, OLR1 - linked to oxLDL- NLRP3 and DECTIN-1 (the latter is the β-Glucan receptor). The most deregulated were OLR1 and DECTIN-1, but in a different way between the two cohorts. In particular, cohort 1 is more deregulated. For inflammatory pathways, however, the same deregulation was not observed in cohort 1 and cohort 2. Cohort 1 tended to be more inflamed than cohort 2, particularly for TNFα, CXCL2, CXCL3 and CXCL8 genes. Following these molecular results, a possible in vitro model was developed. By stimulating Thp1 (immortalized human monocytes) with LPC (main component of oxLDL) a corresponding up-regulation of both cholesterol genes and inflammatory genes (NLRP3, TNFα) was observed, confirming that inflammation and cholesterol travel hand in hand. Finally, on cohort 1 patients analyzed with microarrays, miRNome analysis was carried out and identified miRNAs related to cholesterol genes. In view of these findings, where cohort 1 has been better characterized than cohort 2, it is suggested a personalized approach starting from a molecular signature, in order to define the profile of each patient. In addition, this study suggests that for at least subtypes of patients with MS, statin treatment could be an important aid in improving symptoms.
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Gnoato, Marianna. "Interleuchina-32 ed immunità innata: studio di modelli di flogosi in vitro in cellule epiteliali alveolari e monociti-macrofagi." Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3422659.

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Background IL32 is a recently described proinflammatory cytokine produced by T lymphocytes, natural killer cells, monocytes and epithelial cells. Several studies have demonstrated the importance of IL32 in the regulation of the innate and adaptive immune responses, moreover, it has been found over expressed in inflammatory disorders and in autoimmune diseases. In this project, we focused our attention on studying Chronic Obstructive Pulmonary Disease (COPD) because we think it is a good model for studying the role of IL32 in the innate immunity. Infact, IL32 expression was found to be increased in alveolar macrophages and in lung epithelial cells of smokers with COPD compared to non-smokers. COPD is a chronic respiratory disease characterized by an irreversible limitation on pulmonary airflow associated with chronic inflammation due to several etiological factors such as cigarette smoke. Alveolar epithelial cells and macrophages are primarily involved in its pathogenesis because they secrete cytokines and chemokines recruiting inflammatory cells which sustain the phlogosis. The final effect is lung parenchyma destruction and remodeling . Aim of the study The aim of this study was to investigate the role of IL32 in response to lung injury and in inflammation induced by cigarette smoke. Firstly, ee evaluated if cigarette smoke extract (CSE) was cytotoxic for the lung epithelial cells and macrophages by inducing their apoptosis; then, we investigated if CSE activated epithelial cells by increasing the expression of some proinflammatory cytokines and growth factors. Secondly, we studied if CSE induced IL32 expression by epithelial cells and macrophages and we search for a synergic effect between CSE and other proinflammatory stimuli. Methods For our experiments we employed an alveolar epithelial cell line, A549, and macrophages obtained by THP1 differentiation. Cells were treated with CSE, with PAMPs and IL1β. The PAMPs we used were: polyI:C, imiquimod, MDP and ieDAP.. We evaluated cell viability with Annexin V flow cytometric assay. Moreover, we quantified the mRNA levels of IL32 and other cytokines such as CCL2/MCP1, RAGE and TNF-α with Real Time-PCR. Finally, we investigated IL32 protein expression by Western Blotting and we analyzed its secretion in the conditioned medium from cell cultures with ELISA test. Results We demonstrated that CSE, at low concentration (5%), was able to induce apoptosis of the A549. Moreover, it concurred to their activation by inducing the expression of the proinflammatory CCL2/MCP1 and RAGE and, more importantly, we found that it increased IL32 transcript levels, particularly those of isoform β. In order to test if CSE made epithelial cells more susceptible to the action of other proinflammatory stimuli, cells were treated with CSE together with PAMPs or IL1β. We observed that cells treated with IL1β and CSE showed higher levels of IL32β mRNA compared to those treated with the single stimuli. On the other hand, macrophages resulted to be more resistant to apoptosis induced by CSE dying only at high concentration (20%). Moreover, CSE induced a significant increase of TNF-α expression. More importantly, macrophages treated with CSE showed higher levels of IL32 compared with non-treated cells and this effect resulted to be amplified when they were co-stimulated with IL1β. Discussion These data suggest that cigarette smoke represents an important cytotoxic factor for the epithelium which seems to have a key role in the initial lung injury response. Alveolar epithelial cells activation leads to the production of some factors which recruit macrophages whom trigger the immune response. IL32 seems to be strongly involved in these processes because it is produced both by epithelial cells and macrophages and its expression seems to be enforced by the inflammatory setting
Introduzione L’Interleuchina 32 (IL32) è una citochina proinfiammatoria di recente identificazione prodotta dai linfociti T, dalle cellule natural killer (NK), dai monociti e dalle cellule epiteliali. Essa svolge un ruolo chiave nella regolazione della risposta immunitaria ed è espressa in maniera significativa in alcune patologie infiammatorie croniche e a componente autoimmune. In questo studio, abbiamo identificato nella Broncopneumopatia Cronica Ostruttiva (BPCO) un possibile modello per indagare il ruolo di IL32 nell’infiammazione. Infatti, è stato dimostrato che la sua espressione è elevata nei macrofagi alveolari e nell’epitelio polmonare di soggetti fumatori affetti da BPCO rispetto a quelli non fumatori. La BPCO è una malattia caratterizzata dall’ostruzione irreversibile delle piccole vie aeree e da uno stato di infiammazione cronica del tessuto polmonare dovuto all’azione di vari fattori eziologici tra cui il fumo di sigaretta. Le cellule epiteliali alveolari e i macrofagi alveolari sono primariamente implicati nella patogenesi della BPCO, poiché, in risposta al danno, secernono fattori reclutanti le cellule del sistema immunitario che, in seguito, sostengono la flogosi portando, come conseguenza ultima, alla distruzione e al rimodellamento del parenchima polmonare. Scopo della Tesi Lo scopo di questo studio è stato quello di indagare il ruolo di IL32 nei meccanismi di risposta al danno polmonare e nell’innesco della risposta infiammatoria causati dal fumo. Inizialmente, abbiamo valutato se l’estratto di fumo (CSE) era un fattore citotossico per le cellule epiteliali e per i macrofagi e se induceva la loro apoptosi; inoltre, abbiamo indagato se il fumo contribuiva all’attivazione delle cellule modulando l’espressione, da parte di esse, di citochine e di fattori di crescita proinfiammatori. In seguito, abbiamo studiato se il CSE induceva la produzione di IL32 da parte di queste cellule e se esisteva un effetto sinergico tra la loro azione e quella di altri stimoli proinfiammatori nella modulazione dell’espressione di questa citochina. Materiali e metodi Per gli esperimenti abbiamo utilizzato le cellule epiteliali alveolari di tipo II, A549 e i macrofagi ottenuti dal differenziamento della linea monocitica THP1. Le cellule sono state trattate con il CSE, con i PAMPs e con l’IL1β. I PAMPs utilizzati sono: il polyI:C, l’imiquimod, l’MDP e l’ieDAP. La vitalità cellulare è stata valutata mediante test citofluorimetrico con Annessina V; l'espressione genica di CCL2/MCP1, RAGE, TNF-α e di IL32 è stata effettuata mediante Real Time-PCR. L’espressione proteica di IL32 è stata studiata mediante Western Blotting, mentre la presenza della proteina secreta è stata valutata nel sovranatante delle colture cellulari per mezzo del test ELISA. Risultati: Abbiamo dimostrato che il CSE a basse dosi (5%) era in grado di indurre l’apoptosi delle A549. Oltre a ciò, esso contribuiva alla loro attivazione inducendo un aumento dell’espressione di CCL2/MCP1 e di RAGE e, soprattutto, era in grado di aumentare i livelli di espressione genica di IL32, in particolare, quelli dell’isoforma β. Al fine di testare se il CSE rendeva le A549 più sensibili all’azione di altri fattori proinfiammatori, abbiamo co-trattato le cellule con CSE, con i PAMPs o con IL1β. Abbiamo osservato che le cellule trattate con CSE e IL1β avevano livelli di espressione di IL32β più alti rispetto a quelle trattate con gli stimoli da soli. Dall’altra parte, gli esperimenti condotti sui macrofagi hanno evidenziato che essi erano più resistenti all’apoptosi indotta da CSE, infatti, morivano solo ad alte concentrazioni (20%). Inoltre, il trattamento con CSE induceva un significativo aumento dell’espressione di TNF-α. Oltre a ciò, basse dosi di CSE aumentavano significativamente i livelli di espressione di IL32 e questo effetto risultava amplificato dal co-trattamento con CSE e IL1β. Discussione I dati ottenuti suggeriscono che il fumo rappresenta un importante fattore di citotossicità per l’epitelio il quale sembra avere un ruolo cruciale nelle fasi iniziali di risposta al danno. L’attivazione delle cellule alveolari porta alla produzione di mediatori dell’infiammazione che hanno il compito di reclutare i macrofagi i quali innescano la risposta immunitaria. IL32, sembra essere pesantemente coinvolta nei processi descritti poiché viene prodotta sia dalle cellule epiteliali che dai macrofagi e il contesto infiammatorio contribuisce ad amplificarne l’espressione
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Books on the topic "Monociti"

1

Kellogg, Elizabeth A. Flowering Plants. Monocots. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15332-2.

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Mohlenbrock, Robert H. Filicineae, Gymnospermae, and other monocots, excluding Cyperaceae: Ferns, conifers, and other monocots, excluding sedges. Carbondale, IL: Southern Illinois University Press, 2005.

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Filicineae, Gymnospermae, and other monocots, excluding Cyperaceae: Ferns, conifers, and other monocots, excluding sedges. Carbondale: Southern Illinois University Press, 2005.

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Wilkin, Paul, and Simon J. Mayo, eds. Early Events in Monocot Evolution. Cambridge: Cambridge University Press, 2013. http://dx.doi.org/10.1017/cbo9781139002950.

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Owen, Caroline A. Monocyte adherence to fibronectin: Role of CD11/CD18 integrins and relationship to other monocyte functions. Birmingham: University of Birmingham, 1992.

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Travis, Columbus J., and International Symposium on Grass Systematics and Evolution (4th : 2003 : Ontario, Calif.), eds. Monocots: Comparative biology and evolution : Poales. Claremont, Calif: Rancho Santa Ana Botanic Garden, 2007.

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Simpson, Andrew Wayte. Fibronectin and the regulation of monocyte phagocylosis. Birmingham: Birmingham Polytechnic, 1987.

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International, Conference on the Comparative Biology of the Monocotyledons (3rd 2003 Ontario Calif ). Monocots: Comparative biology and evolution, excluding Poales. Claremont, Calif: Rancho Santa Ana Botanic Garden, 2006.

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Meyers, Stephen C. Flora of Oregon: Pteridophytes, gymnosperms, and monocots. Fort Worth: Botanical Research Institute of Texas Press, 2015.

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Khan, Zeenatul. Adenosine diphosphoribosyl transferase in granulocyte-monocyte differentiation. Uxbridge: Brunel University, 1989.

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Book chapters on the topic "Monociti"

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Pavelka, Margit, and Jürgen Roth. "Monocyte." In Functional Ultrastructure, 348–49. Vienna: Springer Vienna, 2010. http://dx.doi.org/10.1007/978-3-211-99390-3_178.

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Gooch, Jan W. "Monocyte." In Encyclopedic Dictionary of Polymers, 908. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14255.

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Kellogg, Elizabeth A. "Description of the Family, Vegetative Morphology and Anatomy." In Flowering Plants. Monocots, 3–23. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15332-2_1.

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Kellogg, Elizabeth A. "Reproductive Systems." In Flowering Plants. Monocots, 93–101. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15332-2_10.

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Kellogg, Elizabeth A. "Fossil Record and Dates of Diversification." In Flowering Plants. Monocots, 103–7. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15332-2_11.

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Kellogg, Elizabeth A. "Domestication." In Flowering Plants. Monocots, 109–19. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15332-2_12.

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Kellogg, Elizabeth A. "Affinities." In Flowering Plants. Monocots, 121–23. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15332-2_13.

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Kellogg, Elizabeth A. "Subdivision of the Family." In Flowering Plants. Monocots, 127–30. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15332-2_14.

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Kellogg, Elizabeth A. "I. Subfamily Anomochlooideae Pilg. ex Potztal (1957)." In Flowering Plants. Monocots, 131–33. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15332-2_15.

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Kellogg, Elizabeth A. "II. Subfamily Pharoideae L.G. Clark & Judz. (1996)." In Flowering Plants. Monocots, 135–37. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15332-2_16.

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Conference papers on the topic "Monociti"

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Altieri, Dario C., Rossella Bader, and Pier M. Mannucci. "STRUCTURAL DIVERSITY AMONG CELLULAR ADHESION RECEPTORS: FIBRINOGEN BINDING IS A NOVEL BIOLOGICAL PROPERTY OF THE MONOCYTE DIFFERENTIATION ANTIGEN OKM1." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643851.

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A family of related glycoproteins (GP) mediate the interaction between the circulating adhesive proteins and a variety of cells (cytyoadhesins). In this study we have compared two cell-surface antigens which share the property to bind fibrinogen: the platelet GP IIb/IIIa, prototype of the cytoadhesins, and the receptor for fibrinogen costitutively synthesized by monocytes. Two anti-GP IIb/IIIa monoclonal antibodies (Mabs) (LJP9, LJP5), recognizing functionally distinct epitopes of the GP IIb/IIIa did not react with monocytes nor inhibited 125I-fibrinogen binding to monocytes. Similarly, an Arg-Gly-Asp containing peptide which completely abolished platelet-fibrinogen interaction, had no effect on monocytes. Structurally, the monocyte fibrinogen receptor was dimeric and composed of two subunits with molecular weight (Mr) of 155,000 and 95,000. This structural organization was different from that of the GP IIb/IIIa (Mr= 116,000), but in close analogy with the family of leukocyte differentiation antigens OKM1, LFA-1. Therefore, this possible relationship was investigated. A Mab to OKM1 antigen (10 μg/ml) completely suppressed fibrinogen binding to monocytes while it was ineffective on plateles. Iodinated monocyte lysate subjected to immunoprecipitation with OKM1 Mab (60 μg/ml) showed a dimeric antigen with the same molecular size of the monocyte fibrinogen receptor. Moreover, preclearing of the monocyte lysate with OKM1 Mab removed the immunoprecipitate corresponding to the monocyte fibrinogen receptor. These data indicate that the immunologic differentiation antigen OKM1, in addition to function as a complement receptor, displays also the novel biological adhesion property to mediate the binding of fibrinogen to monocytes.
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Kukreti, Sharad, Larry V. McIntire, and C. Wayne Smith. "Molecular Mechanisms of Monocyte Adhesion to Cytokine Stimulated Endothelial Cells Under Physiological Flow Conditions." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0238.

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Abstract This study investigates the underlying mechansisms of monocyte adhesion to both short term (IL-1β, 4 hr) and long term (IL-4, 24 hr) activated endothelial cells. At a wall shear stress of 2 dynes/cm2, monocytes appear to use multiple pathways for primary and secondary adhesion to IL-1β, 4 hr stimulated endothelial cells. However, on IL-4 24 hr stimulated HUVECs, VLA-4/VCAM-1 was the dominant mechanism for monocyte adhesion. Upon additional histamine exposure of IL-4, 24 hr treated endothelial cells, both P-selectin and VLA-4 were involved and had to blocked simultaneously to abolish monocyte adhesion. A combination of IL-1+IL-4 (24 hr) treatment resulted in a complete loss of the primary adhesive mechanism under flow conditions whereas secondary adhesion remained intact as indicated by static experiments.
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Ravi, Arjun, Jonathan Plumb, Jonathan Lemon, George Booth, Jorgen Vestbo, and Dave Singh. "Impaired monocyte chemotaxis in COPD." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa375.

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Moldobaeva, Aigul, Lindsey Eldridge, and Elizabeth Wagner. "Monocyte Differentiation After Ischemic Stress." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1097.

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Jin, Suo, and Don P. Giddens. "Numerical Study of an Asymmetrical Stenosis." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0032.

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Abstract Asymmetrical stenoses are typical in atherosclerosis (1), and it is expected that 3-D flow field effects in the poststenotic region may be significant. Wall shear stress (WSS) which oscillates in direction about a low mean value has been shown to increase the expression of adhesion molecules (VCAM-1, ICAM-1) in cultured endothelial cells, with a consequent increase in monocyte adhesion (2). Thus, the flow field in the vicinity of a raised atherosclerotic lesion may be favorable to monocyte infiltration with subsequent release of matrix-degrading substances (3), leading to plaque rupture.
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Altieri, Dario C., Rossella Bader, and Pier M. Mannucci. "CHARACTERIZATION OF THE FUNCTIONAL ADHESION PROPERTY OF THE MONOCYTE FIBRINOGEN RECEPTOR WITH A MONOCLONAL ANTIBODY (Mab) DIRECTED TO THE ACTIVATED STATE OF THE PLATELET GLYCOPROTEIN (GP) IIb/IIIa." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643849.

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We recently showed that human blood monocytes bind fibrinogen through a genuine surface antigen only in part similar to the platelet GP Ilb/IIIa. Moreover, some anti-GP IIb/IIIa Mabs cross-react with monocytes. In this study we used the 7E3 Mab which preferentially binds to the activated conformation of the platelet GP IIb/IIIa to characterize the dynamic mechanism of "exposure" of the monocyte fibrinogen receptor. 7E3 Mab (25 μg/ml) completely suppressed the binding of i25I-fibrinogen to ADP (10μM)-stimulated monocytes. However, differently from the platelet GP IIb/IIIa, 125I-7E3 binding to unstimulated monocytes was a non-specific and non-saturable reaction. In contrast, after stimulation with ADP (10 μM), suspensions of human monocytes bound 125I-7E3 with saturation of 25-30 μg/ml of added Mab. Scatchard plot analysis was a single-affinity straight line revealing 97,400 binding sites/monocyte with a dissociation constant of 5.2×10−8 M. The monocyte surface antigen uniquely expressed after ADP-activation recognized by 7E3 was visualized by immunoprecipitation studies. Surface iodinated platelet lysate subjected to immunoprecipitation with 7E3 revealed a single band with molecular weight (Mr) of 116,000 corresponding to the platelet GP IIb/IIIa. In contrast, monocytes showed a dimeric surface antigen precipitated by 7E3 in two subunits with Mr=l55,000 and 95,000 respectively. These data indicate that the adhesion properties of the monocyte fibrinogen receptor defined by an anti-platelet GP IIb/IIIa cross-reacting Mab are structurally and functionally distinct from those of the platelet receptor.
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Kozlovskiy, V. "ТРАНСФОРМАЦИЯ МОНОПРОФИЛЬНОГО РЕГИОНАЛЬНОГО ИНДУСТРИАЛИЗМА СЕВЕРО-ЗАПАДА РОССИИ." In Perspektivy social`no-ekonomicheskogo razvitiia prigranichnyh regionov 2019. Институт экономики - обособленное подразделение Федерального исследовательского центра "Карельский научный центр Российской академии наук", 2019. http://dx.doi.org/10.36867/br.2019.31.25.022.

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В статье рассматривается проблема перехода от сложившейся в советское время монопрофильной индустриальной зависимости моногородов СевероЗапада России к их диверсифицированному социальнокультурному и территориальноэкономическому развитию в условиях рыночной экономики. На примере моногородов Архангельской, Вологодской, Ленинградской областей и Республики Карелия, близких в социальнотерриториальном, административном, промышленном устройстве, обнаруживаются значимые социально экономические и культурные различия. The article discusses the problem of the transition from the monoprofile industrial dependence of the monocities of the NorthWest of Russia to the diversified sociocultural and territorialeconomic development in a market economy. On the example of monocities towns of the Arkhangelsk, Vologda, Leningrad regions and the Republic of Karelia, close in the socioterritorial, administrative, industrial structure, are found significant socioeconomic and cultural differences.
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Osteurd, B., J. O. Olsen, and L. Wilsgard. "MONOCYTE STIMULATION IN BLOOD EXPRESSED BY INDUCED THROMBOPLASTIN SYNTHESIS IS CONTROLLED BY THE RELEASE OF ARACHIDONIC ACID AND THE FUNCTION OF PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643289.

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Inhibitors of phoapholipaae A2, block the release of arachidonic acid (20:4) in the cell membrane. Adding such an inhibitor, dibromoacetophenone (20µM) to hepar-inized blood incubated with LPS for 2 hours, blocked totally the induction of thromboplastin synthesis. Liposomes prepared from soyalecithin, containing 60* linoleic acid (18:2) had no stimulatory effect by themselves, but enhanced the stimulating effect of LPS up to 10 fold. When the liposomes were added to the blood samples 0,15,30,60 and 90 min after the LPS had been added, a time dependent response of the liposomes was seen. Blood samples incubated with LPS for 2 hours but only exposed to liposomes for 30 min had monocytes with a thromboplastin activity of 30x10/10-3cells as compared to an activity of 152x10 /10-3 cells in the monocytes of blood incubated with LPS and liposomes for 2 hours. Although the linoleic acid (18:2) is metabolized to arachidonic acid (20:4), it may be more likely that the effect of liposomes is exerted by a mechanism whereby the fatty acid 18:2 is preventing arachidonic acid from being reacylated. This will cause more 20:4 to be free and metabolized to give products required for monocyte activation.A tremendous difference in response to monocyte stimulation between different individuals has been observed. Recently we found that this phenomenon could partially be explained by very active platelets in those with high cell stimuli response. Thus, when platelet rich plasma (PRP) from a high responder was incubated with white cells from a low responder followed by incubation with LPS, there was a drastic increase in monocyte response as compared to the samples where PRP from the low responder was incubated with white cells of its own plus LPS. PRP from a low responder combined with white cells of a high responder resulted in a low response of the monocytes to LPS stimuli.It is concluded that fatty acids and the activity function of platelets may play a central role in monocyte function.
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Carroll, Tomás, Cian O'Leary, Ilaria Ferrarotti, Maurizio Luisetti, Shane O'Neill, and Noel G. McElvaney. "Monocyte Dysfunction In Alpha-1 Antitrypsin Deficiency." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2786.

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Hoogasiam, J., M. Fisher, P. H. Levine, B. W. Weiner, C. H. Vaudreuil, A. Natale, and M. Johnson. "THE EFFECT OF DIETARY COD LIVER OIL SUPPLEMENTATION ON LEUKOCYTE PHYSIOLOGY; A POSSIBLE MEDIATOR OF THE ANTIATHEROGENIC EFFECT OF MARINE OIL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643154.

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Leukocytes appear to be important in the pathophysiology of atherogenesis. Fish oil derived, omega-3 fatty acids suppress atherogenesis in experimental atherosclerosis models and select human populations. We assessed the effect of dietary cod liver oil (CLO) supplementation for 6 weeks on human monocyte and polymorphonuclear leukocyte (PMN) inflammatory potential in healthy controls and patients with a purported autoimmune disorder, multiple sclerosis (MS) in whom monocytes appear to be chronically activated. Baseline and 6 week venous blood samples were obtained from 6 stable MS patients and 6 healthy controls. . Monocyte hydrogen peroxide (HO) production (pMoles/minute/Ix10 monocytes) was measured in a spectrophotofluorometer after stimulation with latex particles. Baseline H2O2 production was 1.551.60 (mean 1 S.D.) in the MS patients and 1.19± .49 in the controls. Post-CLO the values were 1.021.24 and 1.091.27 respectively, representing a significant decline with CLO supplementation in the MS group (P< .01). PMN chemiluminescence (counts x10 /5min/PMN) levels was assessed by a liquid scintillation counter after stimulation with latex particles. Baseline levels were 17.416.1 in the MS group and 17.814.8 in the controls Post-CLO the levels were 12.812.3 and 12.313.3; both signifi-antly lower than baseline (P < .05). PMN superoxide (0 —) levels (nMoles/20min/lxl0 PMN) were measured by the reduction of cyto-chrome-c after stimulation with zymosan. Baseline O2- levels were 21.0±5.8 in the MS group and 22.115.9 in the controls. Post-CLO the O2- levels declined to 8.210.7 and 7.811.5, both significantly lower than baseline (P< .O2-). These data demonstrate that CLO supplementation reduces the intensity of PMN and monocyte reactions to a standard stimulus as measured by toxic oxygen metabolite production, although the monocyte effects were only observed in a population (MS) with increased baseline activity levels.It has previously been assumed that omega-3 fatty acids might exert antiatherogenic effects via their inhibitory effects on platelet reactions. If leukocytes are important mediators of endothelial damage and/or cholesterol deposition in arterial walls, then our data suggest another mechanism by which fish oil may confer benefit in reducing the risk of arterial disease.
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Reports on the topic "Monociti"

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Mozgovaya, E. E., A. S. Trofimenko, M. A. Mamus, E. A. Tikhomirova, S. A. Bedina, and S. S. Spitsma. FORMATION OF MONOCYTE EXTRACELLULAR TRAPS IN RHEUMATOID ARTHRITIS. Academy of Natural Knowledge, 2019. http://dx.doi.org/10.18411/1996-3955-2019-10-86-89.

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Groopman, Jerome E. Pathobiology of HTLV-III/LAV In Human Monocyte-Macrophage. Fort Belvoir, VA: Defense Technical Information Center, April 1990. http://dx.doi.org/10.21236/ada221724.

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Furman, M. I., S. E. Benoit, C. R. Valeri, M. L. Borbonw, and R. C. Becker. Increased Platelet Reactivity and Circulating Monocyte-Platelet Aggregates in Patients with Stable Coronary Artery Disease. Fort Belvoir, VA: Defense Technical Information Center, December 1996. http://dx.doi.org/10.21236/ada360166.

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Murphy, Angus Stuart. Analysis of ABCB phosphoglycoproteins (PGPs) and their contribution to monocot biomass, structural stability, and productivity. Office of Scientific and Technical Information (OSTI), September 2014. http://dx.doi.org/10.2172/1157518.

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Neodo, Anna, Fiona Augsburger, Jan Waskowski, Joerg C. Schefold, and Thibaud Spinetti. Monocytic HLA-DR expression and clinical outcomes in adult ICU patients with sepsis – a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0119.

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Review question / Objective: The scope of this review was defined using PICOTS framework where 1) population: adult critically ill patients with sepsis or septic shock; 2) index prognostic factor: cell surface protein expression of mHLA-DR in blood; 3) comparative factor: none; 4) outcomes to be predicted: mortality, secondary infections, length of stay, and organ dysfunction score (sequential organ failure assessment [SOFA], multiple organ dysfunction score [MODS], logistic organ dysfunction score [LODS]), composite outcomes where component endpoints consist of at least one of the outcomes stated above (e.g., “adverse outcome” defined as death or secondary infection), 5) timing (of the prediction horizon and the moment of prognosis): any; and 6) setting: ICU. Condition being studied: Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to severe infections. It can further progress to septic shock, which includes hemodynamic failure and increased mortality rates. A recent worldwide epidemiological study estimated 48.9 million sepsis cases and 11 million of sepsis-related deaths (~20% of global deaths in 2017). Although its management has advanced considerably, sepsis remains deadly and challenging to treat. The 28/30-day mortality averages around 25% for sepsis and 38% for septic shock in high-income countries. Current models describe the underlying pathophysiologic mechanisms of sepsis as an interplay between concurrent dysfunctional pro- and anti-inflammatory immune response.
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Delmer, Deborah, Nicholas Carpita, and Abraham Marcus. Induced Plant Cell Wall Modifications: Use of Plant Cells with Altered Walls to Study Wall Structure, Growth and Potential for Genetic Modification. United States Department of Agriculture, May 1995. http://dx.doi.org/10.32747/1995.7613021.bard.

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Our previous work indicated that suspension-cultured plant cells show remarkable flexibility in altering cell wall structure in response either to growth on saline medium or in the presence of the cellulose synthesis inhibitor 2,-6-dichlorobenzonitrile (DCB). We have continued to analyze the structure of these modified cell walls to understand how the changes modify wall strength, porosity, and ability to expand. The major load-bearing network in the walls of DCB-adapted dicot cells that lack a substantial cellulose-xyloglucan network is comprised of Ca2+-bridged pectates; these cells also have an unusual and abundant soluble pectic fraction. By contrast, DCB-adapted barley, a graminaceous monocot achieves extra wall strength by enhanced cross-linking of its non-cellulosic polysaccharide network via phenolic residues. Our results have also shed new light on normal wall stucture: 1) the cellulose-xyloglucan network may be independent of other wall networks in dicot primary walls and accounts for about 70% of the total wall strength; 2) the pectic network in dicot walls is the primary determinant of wall porosity; 3) both wall strength and porosity in graminaceous monocot primary walls is greatly influenced by the degree of phenolic cross-linking between non-cellulosic polysaccharides; and 4) the fact that the monocot cells do not secrete excess glucuronoarabinoxylan and mixed-linked glucan in response to growth on DCB, suggests that these two non-cellulosic polymers do not normally interact with cellulose in a manner similar to xyloglucan. We also attempted to understand the factors which limit cell expansion during growth of cells in saline medium. Analyses of hydrolytic enzyme activities suggest that xyloglucan metabolism is not repressed during growth on NaCl. Unlike non-adapted cells, salt-adapted cells were found to lack pectin methyl esterase, but it is not clear how this difference could relate to alterations in wall expansibility. Salt-adaped cell walls contain reduced hyp and secrete two unique PRPP-related proteins suggesting that high NaCl inhibits the cross-linking of these proteins into the walls, a finding that might relate to their altered expansibility.
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Peng, Liang, Baodi Cao, Fangpeng Hou, Baolin Xu, Baolin Xu, Luyi Liang, Yu Jiang, Xiaohui Wang, and Jingjian Zhou. Relationship between platelet to lymphocyte ratio (PLR) and lymphocyte to monocyte ratio (LMR) with spontaneous preterm birth: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2022. http://dx.doi.org/10.37766/inplasy2022.3.0092.

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Freeman, Stanley, Russell Rodriguez, Adel Al-Abed, Roni Cohen, David Ezra, and Regina Redman. Use of fungal endophytes to increase cucurbit plant performance by conferring abiotic and biotic stress tolerance. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7613893.bard.

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Major threats to agricultural sustainability in the 21st century are drought, increasing temperatures, soil salinity and soilborne pathogens, all of which are being exacerbated by climate change and pesticide abolition and are burning issues related to agriculture in the Middle East. We have found that Class 2 fungal endophytes adapt native plants to environmental stresses (drought, heat and salt) in a habitat-specific manner, and that these endophytes can confer stress tolerance to genetically distant monocot and eudicot hosts. In the past, we generated a uv non-pathogenic endophytic mutant of Colletotrichum magna (path-1) that colonized cucurbits, induced drought tolerance and enhanced growth, and protected 85% - 100% against disease caused by certain pathogenic fungi. We propose: 1) utilizing path-1 and additional endophtyic microorganisms to be isolated from stress-tolerant local, wild cucurbit watermelon, Citrulluscolocynthis, growing in the Dead Sea and Arava desert areas, 2) generate abiotic and biotic tolerant melon crop plants, colonized by the isolated endophytes, to increase crop yields under extreme environmental conditions such as salinity, heat and drought stress, 3) manage soilborne fungal pathogens affecting curubit crop species growing in the desert areas. This is a unique and novel "systems" approach that has the potential to utilize natural plant adaptation for agricultural development. We envisage that endophyte-colonized melons will eventually be used to overcome damages caused by soilborne diseases and also for cultivation of this crop, under stress conditions, utilizing treated waste water, thus dealing with the limited resource of fresh water.
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Cohen, Yuval, Christopher A. Cullis, and Uri Lavi. Molecular Analyses of Soma-clonal Variation in Date Palm and Banana for Early Identification and Control of Off-types Generation. United States Department of Agriculture, October 2010. http://dx.doi.org/10.32747/2010.7592124.bard.

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Date palm (Phoenix dactylifera L.) is the major fruit tree grown in arid areas in the Middle East and North Africa. In the last century, dates were introduced to new regions including the USA. Date palms are traditionally propagated through offshoots. Expansion of modern date palm groves led to the development of Tissue Culture propagation methods that generate a large number of homogenous plants, have no seasonal effect on plant source and provide tools to fight the expansion of date pests and diseases. The disadvantage of this procedure is the occurrence of off-type trees which differ from the original cultivar. In the present project we focused on two of the most common date palm off-types: (1) trees with reduced fruit setting, in which most of the flowers turn into three-carpel parthenocarpic fruits. In a severe form, multi-carpel flowers and fruitlets (with up to six or eight carpels instead of the normal three-carpel flowers) are also formed. (2) dwarf trees, having fewer and shorter leaves, very short trunk and are not bearing fruits at their expected age, compared to the normal trees. Similar off-types occur in other crop species propagated by tissue culture, like banana (mainly dwarf plants) or oil palm (with a common 'Mantled' phenotype with reduced fruit setting and occurrence of supernumerary carpels). Some off-types can only be detected several years after planting in the fields. Therefore, efficient methods for prevention of the generation of off-types, as well as methods for their detection and early removal, are required for date palms, as well as for other tissue culture propagated crops. This research is aimed at the understanding of the mechanisms by which off-types are generated, and developing markers for their early identification. Several molecular and genomic approaches were applied. Using Methylation Sensitive AFLP and bisulfite sequencing, we detected changes in DNA methylation patterns occurring in off-types. We isolated and compared the sequence and expression of candidate genes, genes related to vegetative growth and dwarfism and genes related to flower development. While no sequence variation were detected, changes in gene expression, associated with the severity of the "fruit set" phenotype were detected in two genes - PdDEF (Ortholog of rice SPW1, and AP3 B type MADS box gene), and PdDIF (a defensin gene, highly homologous to the oil palm gene EGAD). We applied transcriptomic analyses, using high throughput sequencing, to identify genes differentially expressed in the "palm heart" (the apical meristem and the region of embryonic leaves) of dwarf vs. normal trees. Among the differentially expressed genes we identified genes related to hormonal biosynthesis, perception and regulation, genes related to cell expansion, and genes related to DNA methylation. Using Representation Difference Analyses, we detected changes in the genomes of off-type trees, mainly chloroplast-derived sequences that were incorporated in the nuclear genome and sequences of transposable elements. Sequences previously identified as differing between normal and off-type trees of oil palms or banana, successfully identified variation among date palm off-types, suggesting that these represent highly labile regions of monocot genomes. The data indicate that the date palm genome, similarly to genomes of other monocot crops as oil palm and banana, is quite unstable when cells pass through a cycle of tissue culture and regeneration. Changes in DNA sequences, translocation of DNA fragments and alteration of methylation patterns occur. Consequently, patterns of gene expression are changed, resulting in abnormal phenotypes. The data can be useful for future development of tools for early identification of off-type as well as for better understanding the phenomenon of somaclonal variation during propagation in vitro.
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Firon, Nurit, Prem Chourey, Etan Pressman, Allen Hartwell, and Kenneth J. Boote. Molecular Identification and Characterization of Heat-Stress-Responsive Microgametogenesis Genes in Tomato and Sorghum - A Feasibility Study. United States Department of Agriculture, October 2007. http://dx.doi.org/10.32747/2007.7591741.bard.

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Exposure to higher than optimal temperatures - heat-stress (HS) - is becoming increasingly common to all crop plants worldwide. Heat stress coinciding with microgametogenesis, especially during the post-meiotic phase that is marked by starch biosynthesis, is often associated with starch-deficient pollen and male sterility and ultimately, greatly reduced crop yields. The molecular basis for the high sensitivity of developing pollen grains, on one hand, and factors involved in pollen heat-tolerance, on the other, is poorly understood. The long-term goal of this project is to provide a better understanding of the genes that control pollen quality under heat-stress conditions. The specific objectives of this project were: (1) Determination of the threshold heat stress temperature(s) that affects tomato and sorghum pollen quality whether: a) Chronic mild heat stress conditions (CMHS), or b) Acute heat stress (AHS). (2) Isolation of heat-responsive, microgametogenesis-specific sequences. During our one-year feasibility project, we have accomplished the proposed objectives as follows: Objectrive 1: We have determined the threshold HS conditions in tomato and sorghum. This was essential for achieving the 2nd objective, since our accumulated experience (both Israeli and US labs) indicate that when temperature is raised too high above "threshold HS levels" it may cause massive death of the developing pollen grains. Above-threshold conditions have additional major disadvantages including the "noise" caused by induced expression of genes involved in cell death and masking of the differences between heatsensitive and heat-tolerant pollen grains. Two different types of HS conditions were determined: a) Season-long CMHS conditions: 32/26°C day/night temperatures confirmed in tomato and 36/26°C day maximum/night minimum temperatures in sorghum. b) Short-term AHS: In tomato, 2 hour exposure to 42-45°C (at 7 to 3 days before anthesis) followed by transfer to 28/22±2oC day/night temperatures until flower opening and pollen maturation, caused 50% reduced germinating pollen in the heat-sensitive 3017 cv.. In sorghum, 36/26°C day/night temperatures 10 to 5 days prior to panicle emergence, occurring at 35 days after sowing (DAS) in cv. DeKalb28E, produced starch-deficient and sterile pollen. Objective 2: We have established protocols for the high throughput transcriptomic approach, cDNA-AFLP, for identifying and isolating genes exhibiting differential expression in developing microspores exposed to either ambient or HS conditions and created a databank of HS-responsivemicrogametogenesis-expressed genes. A subset of differentially displayed Transcript-Derived Fragments (TDFs) that were cloned and sequenced (35 & 23 TDFs in tomato and sorghum, respectively) show close sequence similarities with metabolic genes, genes involved in regulation of carbohydrate metabolism, genes implicated in thermotolerance (heat shock proteins), genes involved in long chain fatty acids elongation, genes involved in proteolysis, in oxidation-reduction, vesicle-mediated transport, cell division and transcription factors. T-DNA-tagged Arabidopsis mutants for part of these genes were obtained to be used for their functional analysis. These studies are planned for a continuation project. Following functional analyses of these genes under HS – a valuable resource of genes, engaged in the HS-response of developing pollen grains, that could be modulated for the improvement of pollen quality under HS in both dicots and monocots and/or used to look for natural variability of such genes for selecting heat-tolerant germplasm - is expected.
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