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Hamon, Yveline. "Mise en évidence d'une altération fonctionnelle du récepteur soluble de l'immunité innée PTX3 dans la mucoviscidose." Phd thesis, Université d'Angers, 2013. http://tel.archives-ouvertes.fr/tel-00843818.
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La pentraxine longue PTX3, récepteur soluble de l'immunité innée, joue un rôle important dans la protection contre certains pathogènes, en favorisant leur élimination et l'initiation de réponses immunitaires protectrices. PTX3 a notamment un rôle protecteur lors d'infections par Aspergillus fumigatus et Pseudomonas aeruginosa. La mucoviscidose, maladie héréditaire grave à transmission autosomique récessive, est caractérisée par des infections pulmonaires récurrentes, notamment par ces deux pathogènes. Nous avons donc émis l'hypothèse que le statut de PTX3 pourrait être altéré chez ces patients. L'expression et l'intégrité de PTX3 ont été analysées dans les expectorations de 51 patients atteints de mucoviscidose et de 7 patients atteints de broncho-pneumopathie chronique obstructive (BPCO). Les résultats montrent que la concentration de PTX3 est augmentée dans les sérums de patients atteints de mucoviscidose. Au contraire, la concentration de PTX3 dans les expectorations de patients atteints de mucoviscidose est considérablement plus faible que celle des patients atteints de BPCO. Cette faible concentration de PTX3 résulte d'un clivage protéolytique par l'élastase du neutrophile et par les protéases sécrétées par Aspergillus fumigatus. De manière intéressante, le domaine N-terminal de PTX3, impliqué dans la protection contre Aspergillus fumigatus, est préférentiellement dégradé par ces protéases. Cette dégradation est spécifique de la pentraxine longue PTX3 car les pentraxines courtes, CRP et SAP, ne sont pas dégradées. Ces résultats indiquent que la protéolyse sélective de PTX3 au niveau des voies respiratoires des patients atteints de mucoviscidose peut expliquer, en partie, les infections pulmonaires récurrentes par certains pathogènes.
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Jaillon, Sébastien. "Nouveaux sites d'expression et rôles fonctionnels de Pentracine 3, récepteur soluble de l'immunité innée." Angers, 2007. http://www.theses.fr/2007ANGE0064.
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Le système immunitaire est constitué de deux composantes : l'immunité innée et l'immunité adaptative. Alors que le système immunitaire adaptatif utilise des récepteurs spécifiques pour la reconnaissance des antigènes, les récepteurs utilisés par l'immunité innée sont appelés « Pattern Recognition Receptors 1 » ou PPR. Les PRRs reconnaissent des motifs hautement conservés durant l'évolution, exprimés exclusivement par les microorganismes et appelés « Pathogen Associated Molecular Pattern » ou PAMP. Les PRRs sont composés des PRRs associés aux cellules (impliqués dans l'endocytose et/ou la signalisation) et des PRRs solubles qui facilitent l'élimination des microorganismes (non soi) et des cellules apoptotiques (soi modifié). Appartenant à la famille des PRRs solubles, les pentraxines sont divisées en deux sous-familles sur la base de leur structure primaire : les pentraxines courtes (protéines de la phase aigüe de l'inflammation CRP et SAP) et les pentraxines longues dont la molécule pentraxine 3 (PTX3). PTX3 fixe de nombreux pathogènes (A. Fumigatus, P. Aeruginosa) et est impliqué dans la protection contre ces microorganismes et dans la régulation de la réponse inflammatoire. Nous avons démontré que les neutrophiles, premières cellules à intervenir au niveau d’un foyer infectieux, contiennent un stock préformé de PTX3 rapidement mobilisable lors d'une stimulation par des microorganismes ou des agonistes des TLRs. PTX3 est également retrouvé au niveau des « Extracellular Traps » ou NET qui piègent et éliminent les microorganismes. De plus, PTX3 contenu dans les neutophiles est primordial pour le contrôle in vivo d'une infection par A. Fumigatus. Nous avons ensuite démontré la relocalisation membranaire de PTX3 lors de l'apoptose du neutrophile indépendamment de sa dégranulation. Le blocage de PTX3 membranaire par un anticorps inhibe la reconnaissance des neutrophiles apoptotiques par les macrophages. Ainsi, alors que plusieurs travaux démontrent que la forme soluble se fixe aux cellules apoptotiques et inhibe leur élimination, la relocalisation de PTX3 à la membranaire des neutrophiles apoptotiques, participerait à la résolution de l'inflammation. Finalement, nous avons mis en évidence la présence de PTX3 dans le colostrum humain, indépendante d'une augmentation systémique de sa concentration. Un déficit de production de PTX3 par les cellules du nouveau-né pourrait ainsi être comblé par un apport maternel lors de l'allaitement. L'ensemble de ces travaux précise les modalités de production et de régulation de PTX3 dans les phases précoces de l'inflammation et étendent son rôle dans les mécanismes de résolution de l'inflammation et de l'immunité néonataleImmune system is divided into innate and adaptative immunity. Receptors used by adaptative -- are specific for the pathogen recognition compared with these used by innate immunity called « Pattern Recognition Receptor" or PRR. PRR recognize highly conserved motifs expressed by micoorganisms and called "Pathogens Associated Molecular Patterns" or PAMP. Based on their localisation, PRR are sub-divided into two groups (i) cell-associated PRR (e. G. Endocytic PRR and signaling PRR) and (ii) soluble PRR which recognize and facilitate the clearence of microorganisms (rot self) and apoptotic cells (altered self). Belonging to the soluble PRR family, pentraxins are divided in two sub-families based on their primary structure: the short pentraxin (acute phase proteins C-Reactive Protein (CRP) and Serum Amyloid-P (SAP)) and the long pentraxins which peantraxin 3 (PTX3) is the prototypic member. PTX3 binds numerous pathogens (e. G. A. Fumigatus, P. Aeruginosa) and is involved in the protection against these microorganisms and in the control of inflammation. We showed that neutrophils, the first cells recruited at the infection sites, contain a preformed stock of PTX3 ready for rapid release upon stimulation with microorganisms or TLR agonists. PTX3 is also found in the Neutrophil Extracellular Traps (NET) generated upon neutrophil stimulation. Moreover, neutrophil-associared-PTX3 is required for the in vivo control of A. Fumigatus infection. We have also demonstrated that PTX3 relocalizes at the membrane of apoptotic neutrophils independently of their degranulation. Blocking PTX3 inhibits the recognition of apoptotic neutrophils by phagocytes. While soluble PTX3 binds apoptotic neutrophils and inhibits their clearence by macrophages, membrane relocalisation of endogenous PTX3 may participate to the resolution of inflammation. Finally, we showed the presence ot PTX3 in human colostrum independently of an increased of systemic concentration. A deficit in PTX3 production by neonate cells could be filled by milk suckling. Collectively, these data provide original informations on the regulation of PTX3 production in the early phase of inflammation and extend its role in the resolution of inflammation and in neonate immunity
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Gifoni, Markus Andret Cavalcante. "Envolvimento da pentraxina 3 (PTX3) na patogÃnese da cistite hemorrÃgica induzida por ifosfamida em camundongos." Universidade Federal do CearÃ, 2008. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=1245.
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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel SuperiorA cistite hemorrÃgica (CH) à um fenÃmeno inflamatÃrio frequentemente associado à quimioterapia com oxazafosforinas. Trata-se de uma resposta inflamatÃria inata à aÃÃo da AcroleÃna (ACR), metabÃlito hepÃtico comum à Ifosfamida (IFO) e à ciclofosfamida (CTX). O papel da resposta ao recrutamento de receptores toll-like (TLR) e do estÃmulo por TNF-α e IL-1β com envolvimentto de iNOS e COX-2 tem sido demonstrado neste fenÃmeno. Estudos recentes demonstram que a Pentraxina 3 (PTX3) assume papel de mediador inflamatÃrio em modelos de resposta inflamatÃria inata in vivo, sobretudo relacionada ao recrutamento de TLR. Desta forma, o presente estudo pretende investigar o possÃvel envolvimento de PTX3 na patogÃnese da CH induzida por ifosfamida em camundongos. Para isso, foi realizada quantificaÃÃo de RNAm por RT-PCR para PTX3 e IL-1β em camundongos C57/ BL6 tratados com ifosfamida e salina. Em seguida, o modelo experimental da CH induzida por ifosfamida foi reproduzido em grupos de camundongos com hiperexpressÃo e nocauteados para PTX3 em comparaÃÃo com os respectivos controles do tipo selvagem e com grupos controle tratados com salina para posterior obtenÃÃo dos pesos vesicais Ãmidos (PVU), realizaÃÃo de anÃlise histomorfomÃtrica, imunohistoquÃmica e quantificaÃÃo de RNAm por RT-PCR para PTX3, IL-1β, TNF-α e iNOS. Os animais transgÃnicos e seus controles foram sacrificados com tempos de 3h e 12h apÃs o tratamento, enquanto os nocauteados e seus controles foram sacrificados com 12 horas do tratamento. Finalmente, a CH em animais C57/ BL6 foi modulada com o prÃ-tratamento com Talidomida, Pentoxifilina, MESNA, Amifostina e Aminoguanidina para a posterior marcaÃÃo imunohistoquÃmica com PTX3, IL-1β, TNF-α e iNOS. Observou-se que o RNAm de PTX3 està cerca de 70 vezes mais expresso em animais com CH, contra uma razÃo de expressÃo de 10 para IL-1β. Animais trangÃnicos para PTX3 tÃm reduÃÃo inicial da resposta inflamatÃria com expressÃo inferior de PTX3 e TNF-α e expressÃo aumentada de iNOS e intensificaÃÃo da inflamaÃÃo ao tempo de 12 horas, com expressÃo superior dos mediadores. NÃo houve diferenÃas significativas de intensidade da CH em animais KO em relaÃÃo aos controles. A modulaÃÃo da CH por talidomida e MESNA produziu reduÃÃo importante sobre a expressÃo de PTX3, enquanto a inibiÃÃo da CH por amifostina nÃo teve reduÃÃo expressiva da pentraxina. Em conjunto, estes dados apontam para um envolvimento inequÃvoco de PTX3 na fisiopatologia da inflamaÃÃo inata em modelo de CH murino com Ãntima relaÃÃo coma expressÃo de TNF-α
The Hemorrhagic Cystitis (HC) is an inflammatory reaction usually associated with Cancer Chemotherapy with Oxazaphosphorines. It is an innate inflammatory response to vesical irritation by Acrolein, an hepatic metabolite of the treatment with Iphosphamide and Cyclophosphamide. The role of toll-like receptor (TLR) engagement and TNF-α and IL-1β expression and the involvement of iNOS and COX-2 in the pathogenesis has been well demonstrated in a murine model of HC. Recent data configure pentraxin 3 (PTX3) as an inflammatory mediator in several experimental models of innate immune response in vivo, with a straight relation with TLR engagement. Because of that, this study looks at the involvement of PTX3 in the pathogenesis of iphosphamideâinduced HC in mice. For this purpose, the mRNA to PTX3 and IL-1β t was quantified by RT-PCR in groups of C57BL6 mice treated with Iphosphamide or Saline. After that, groups of transgenic and Knock-Out mice to PTX3 and its respectives wild-type controls were treated with Iphosphamide or saline with intention to measure the Bladder Wet Weight (BWW), histomorphometric scores and Immunohistochemistry and RT-PCR to PTX3, IL-1β, TNF-α e iNOS analysis. The transgenic mice and its controls were killed in 3h and 12h after the treatment, while the PTX3 KO and its controls were killed after 12 hours. Finally, the experimental HC was modulated by pretreatment with Talidomide, Pentoxiphiline, MESNA, Amifostine and Aminoguanidine and the bladders submitted to immunohistochemistry assay (PTX3, TNF-α, IL-1β and iNOS). By RT-PCR quantification, mRNA for PTX3 was expressed 70 times more in mice treated with iphosphamide than in controls, while IL-1β RNAm had an expression rate of 10 times. PTX3 transgenic mice had initial reduction of the inflammatory response with less expression of PTX3 and TNF-α and greater expression of iNOS. In the other hand, after 12 hours, the PTX3 transgenic mice had more inflammatory signs with superior expression of all the mediators. There was no difference between the PTX3 KO mice and its controls in the HC intensity although differences between groups were seen in cytokines expression. Talidomide and MESNA produced substantial reduction on the PTX3 expression, the same was seen to TNF-α, while the amifostine marked inhibition of HC had low effect on PTX3 expression. These data as a whole, point to an unequivocal involvement of PTX3 in the pathogenesis of innate inflammatory response of HC in mice with close relation with TNF-α engagement
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Junqueira, Ana FlÃvia Torquato de AraÃjo. "Estudo do efeito do inibidor da enzima adenosina desaminase, EHNA, sobre a enterite induzida pela toxina a do Clostridium difficile em alÃa ileal isolada de camundongos." Universidade Federal do CearÃ, 2008. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=1305.
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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgicoO Clostridium difficile tem como principal fator de virulÃncia a toxina A (TxA), a qual provoca inflamaÃÃo e destruiÃÃo tecidual aguda em intestinos de animais experimentais e de pacientes com a doenÃa induzida por esta bactÃria. Em locais de injÃria tecidual, adenosina à produzida em altas concentraÃÃes, onde exerce uma sÃrie de efeitos antiinflamatÃrios, limitados por sua rÃpida degradaÃÃo pela enzima adenosina desaminase. O objetivo deste trabalho foi investigar o efeito da inibiÃÃo da enzima adenosina desaminase pelo EHNA (eritro-9-(2-hidrÃxi-3-nonil)-adenina) sobre a enterite induzida pela TxA do C. difficile em alÃa ileal de camundongos. Para isto, injetamos EHNA (90 μmol/kg) ou PBS i.p. 30 minutos antes da administraÃÃo de TxA (10 a 100 μg) ou PBS na alÃa ileal isolada. Os animais foram sacrificados 3 horas depois da induÃÃo da enterite e as alÃas foram retiradas para estudo. As razÃes peso/comprimento da alÃa e volume de secreÃÃo/comprimento da alÃa foram calculadas e amostras de tecido foram coletadas para histopatologia, dosagem de atividade de mieloperoxidase (MPO), dosagem de TNF-α, IL-1β e IL-10 por ELISA, imunohistoquÃmica para TNF-α, IL-1β, NOS induzÃvel e PTX3, e PCR para TNF-α, IL-1β e PTX3. A injeÃÃo de TxA (10 a 100 μg) nas alÃas ileais aumentou significativamente (p<0,05) as razÃes peso/comprimento da alÃa e volume de secreÃÃo/comprimento da alÃa com resultados consistentes a partir de 50 μg. A TxA promoveu significativa (p<0,05) destruiÃÃo tecidual, edema, infiltraÃÃo de cÃlulas inflamatÃrias, aumento das citocinas TNF-α e IL-1β, e elevaÃÃo de iNOS e PTX3. Todos esses parÃmetros foram significativamente revertidos com o uso do EHNA (p<0,05). Em adiÃÃo, a TxA nÃo alterou os nÃveis de IL-10 em relaÃÃo ao controle, mas o prÃ-tratamento com EHNA promoveu uma elevaÃÃo nos nÃveis desta citocina. Assim, concluÃmos que na enterite induzida pela TxA em camundongos o EHNA demonstrou um potente efeito antiinflamatÃrio, reduzindo consideravelmente a lesÃo tecidual, a migraÃÃo neutrofÃlica, a expressÃo e os nÃveis de citocinas prÃinflamatÃrias (TNF-α, IL-1β) e produzindo um aumento nos nÃveis de IL-10. AlÃm disso, a administraÃÃo de TxA induziu um aumento na expressÃo da proteÃna PTX3 e no nÃmero de cÃlulas imunomarcadas para iNOS no tecido ileal, ambos revertidos pelo EHNA
The main factor of virulence in Clostridium difficile is toxin A (TxA), which can induce inflammation and acute tissue injury in the bowels of animals and humans affected by this organism. The high concentration of adenosine generated upon injury produces a number of antiinflammatory effects limited by rapid degradation by adenosine deaminase. The objective of this study was to determine the effect of EHNA (erythro-9-(2-hydroxy-3-nonyl)-adenine) inhibition of adenosine deaminase upon TxA-induced ileal loop enteritis in mice. EHNA (90 μmol/kg) or PBS was injected i.p. 30 minutes prior to TxA (10-100 μg) or PBS instillation into the ligated ileal loop. The animals were euthanized 3 hours after enteritis induction and the ileal loops were retrieved for analysis. The weight/length ratio and the secretion volume/length ratio were calculated and tissue samples were submitted to histopathological study, myeloperoxidase assay (MPO), measurement of TNF-α, IL-1β and IL-10 levels with ELISA, immunohistochemical tests for TNF-α, IL-1β, inducible NOS and PTX3, and PCR assay for TNF-α, IL-1β and PTX3. The instillation of TxA (10-100 μg) into the ileal loop significantly increased (p<0.05) the weight/length ratio and the secretion volume/length ratio with consistent results above 50 μg. TxA induced a significant amount (p<0.05) of histological damage, edema and inflammatory cell infiltration and increased the production of TNF-α, IL-1β, iNOS and PTX3. All changes were significantly reverted by treatment with EHNA (p<0.05). Moreover, IL-10 levels remained unchanged in animals treated with TxA, but increased in animals receiving EHNA. In conclusion, in mice with TxA-induced enteritis EHNA produced considerable antiinflammatory effects, reducing tissue injury, neutrophil migration, the expression and levels of proinflammatory cytokines (TNF-α and IL-1β) and producing an increase in IL-10 levels. In addition, TxA instillation increased PTX3 expression and the number of cells immunolabeled for iNOS in the ileal tissue, both of which were reverted by EHNA
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Rodrigues, Priscila Fabiana. "Avaliação do efeito da proteína Pentraxina 3 em células tumorais murinas." Universidade Federal de Minas Gerais, 2014. http://hdl.handle.net/1843/BUOS-9MKKQ3.
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Pentraxin 3 (PTX3) is an inflammatory protein that plays important role in innate immunity, matrix deposition and female fertility. Moreover, it is a natural antagonist of fibroblast growth factor 2 (FGF2) that inhibit the cellular proliferation and angiogenesis promoted by this factor. PTX3 binds to FGF2 in the site of interaction with its receptor (FGFR) preventing the activation of FGF2/FGFR signaling pathway and, as a consequence, inhibiting the expression of genes related to cell proliferation, migration, differentiation, survival and angiogenesis. Neoplasms are among the leading causes of death worldwide and the estimatives point to an increase in incidence of this type of disease. The FGF signaling pathway is crucial in tumor biology by regulating essential processes in tumorigenesis, as cell proliferation and angiogenesis. The identification of inhibitors of this pathway is important for the understanding of the biology of cancer and for the development of therapeutic approaches aimed at controlling growth and tumor progression. The objective of this study was to evaluate the biological effect of PTX3 in murine tumor cell lines derived from melanocytic melanoma (B16F10 and B16F1), amelanocytic melanoma (K1735 and K1735 M2) and fibrosarcoma (MC-TGS17-51 and Sal/N). The morphology of the cells was assessed by optical phase contrast microscopy and the structure of the actin cytoskeleton by immunofluorescence. Cell proliferation was evaluated by MTT assay and gene expression profile was measured by RT-PCR. Under our experimental conditions, PTX3 did not promote morphological changes or in the pattern of organization of actin in the cells K1735 M2 and B16F1. A higher number of viable cells compared to control was observed in response to the treatment with PTX3 in all types of cells. The expression of the FGF receptors (FGFR) 1, 3 and 4 was verified in all cells but the expression of FGFR2 was detected only in the lineage of fibrosarcoma Sal/N. Ptx3 was expressed by almost all cell lines but not by K1735 melanoma. No FGF2 basal expression was observed in B16F1 melanoma. Our data corroborate the findings of lack of expression of FGFR2 in tumors, particularly melanomas. We show here, for the first time, the expression of PTX3 in murine fibrosarcomas and melanomas. The results presented here contribute to the functional characterization of PTX3 and point out the need for studies aiming the evaluation of its role in the tumor microenvironment and the potencial usage of PTX3 as a biomarker for the diagnosis and prognosis of tumors.Pentraxina 3 (PTX3) é uma importante proteína inflamatória, componente essencial da resposta imune inata, com função também na deposição de matriz e fertilidade feminina. Além disso, ela também é capaz de se ligar ao fator de crescimento de fibroblasto 2 (FGF2) e inibir as atividades biológicas de indução da proliferação celular e angiogênese promovidas por esse fator. PTX3 se liga a FGF2 no sítio de interação com o seu receptor (FGFR) e impede que a ligação FGF2/FGFR ocorra e, consequentemente, vias de sinalização que ativam genes ligados à proliferação celular, migração, diferenciação, sobrevivência e angiogênese não são ativadas. As neoplasias figuram entre as principais causas de morte mundiais e as estimativas apontam para um aumento de sua incidência no mundo todo. A via de sinalização de FGF é importante na biologia dos tumores por regular a proliferação celular e a angiogênese, processos essenciais para o crescimento e desenvolvimento tumoral. A identificação de inibidores desta via é importante para o entendimento da biologia do câncer e para o desenvolvimento de abordagens terapêuticas visando controlar o crescimento e a progressão tumoral. PTX3 é um antagonista natural de FGF2 que, além de inibir a proliferação celular e a angiogênese induzidas por esse fator, também é capaz de diminuir o crescimento e volume tumoral in vivo. O objetivo deste trabalho foi avaliar o efeito biológico de Ptx3 em linhagens de células tumorais murinas derivadas de melanoma melanocítico (B16F10 e B16F1), melanoma amelanocítico (K1735 e K1735 M2) e fibrosarcoma (MC-TGS17-51 e Sal/N). A morfologia das células foi avaliada por microscopia óptica de contraste de fase e a estrutura do citoesqueleto de actina por imunofluorescência. A proliferação celular foi analisada pelo método MTT e o padrão de expressão de genes por RT-PCR. Nas condições dos nossos ensaios, o tratamento com Ptx3 não promoveu mudanças morfológicas nas células ou no padrão de organização da actina nas linhagens K1735 M2 e B16F1. Um maior número de células viáveis em comparação com o controle foi observado nas células tratadas com Ptx3. Foi verificado que todas as linhagens expressam os receptores Fgfr1, 3 e 4. Já a expressão do receptor Fgfr2 foi observada apenas na linhagem de fibrosarcoma Sal/N. Somente a linhagem de melanoma K1735 não apresentou expressão basal de Ptx3 e a linhagem B16F1 a expressão de Fgf2. Nossos dados corroboram os achados de ausência de expressão de Fgfr2 nos tumores, especialmente nos melanomas, e mostram de forma inédita a expressão de Ptx3 em linhagens murinas de fibrosarcomas e melanomas. Os resultados aqui apresentados contribuem para a caracterização funcional de PTX3, e apontam a necessidade de estudos buscando avaliar o seu papel no microambiente tumoral e a possibilidade do seu uso como biomarcador no diagnóstico diferencial e prognóstico de tumores.
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Flatscher, Katharina. "Stellenwert von Pentraxin-3 als diagnostischer Marker für die Prädiktion der Präeklampsie." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-170954.
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Nunes, João Paulo Silva. "Avaliação do efeito biológico da pentraxina 3 em linhagens de células tumorais humanas." Universidade Federal de Minas Gerais, 2014. http://hdl.handle.net/1843/BUOS-9KWJP6.
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The pentraxin 3 is an acute phase glycoprotein expressed in a wide variety of cells and plays a myriad of roles in biological processes including female fertility, innate immunity and angiogenesis. PTX3 interacts selectively and specifically to fibroblast growth factors (FGFs) preventing the engagement of these factors with their specific tyrosine kinase receptors (FGFRs). The FGF/FGFR system plays important roles in many processes such as migration, differentiation, survival and cell proliferation, and in angiogenesis. Angiogenesis contributes to the development and progression of a variety of physiological and pathological conditions. In cancer, the formation of new vascular channels favors the proliferation of tumor cells, local invasion and metastasis. The possibility of modulating angiogenesis by altering the balance between pro- and anti-angiogenic factors therefore has great therapeutic potential. In this sense, studies aiming the identification and functional characterization of molecules such as PTX3, which is a natural antagonist of FGF/FGFR system, are very important. The objectives of this study were to characterize the expression of PTX3 in human cells derived from sarcoma (HT 1080, SAOS 2), colon (HCT 116, CACO 2 and SW 480) and melanoma (SK-MEL 37 and SK-MEL 188) and to evaluate its effect on cell proliferation and expression of genes related to inflammatory response and angiogenesis. Gene expression profile was investigated by RT-PCR and cell proliferation assessed by MTT assay and by counting cells stained with Trypan Blue dye. Morphology was observed by contrast phase optical microscopy and immunofluorescence using rhodamine-phalloidin conjugated to TRITC to assess F-actin filaments. We found that tumor cell lines HT 1080, HCT 116, SK-MEL 37 and SK-MEL 188 express FGF 2 and all the FGF receptors investigated (FGFR 1-4). None of the cells expressed FGF8. PTX3 basal expression was observed in HT 1080, HCT 116, SK-MEL 188 e CACO 2 lines. Preliminary results indicate that PTX3 impair the proliferation of human fibrosarcoma HT 1080 cells. By immunofluorescence, we found that PTX3 seems to interfere with the structure of actin filaments, and reduces the number of filopodia in HT 1080 cells and human colorectal adenocarcinoma HCT 116 cells. These results indicate the need for further investigation of the role of PTX3 in FGF -dependent human tumor cells migration and proliferation as well as for the evaluation of the therapeutic potential of PTX3 as an anti - angiogenic tool.A pentraxina 3 é uma glicoproteína de fase aguda expressa em uma grande variedade de células e que desempenha uma miríade de funções em processos biológicos associados a fertilidade feminina, imunidade inata e angiogênese. PTX3 interage seletivamente e especificamente aos fatores de crescimento de fibroblastos (FGFs) impedindo a interação desses fatores com seus receptores específicos do tipo tirosina quinase (FGFR) presentes na membrana das células. O sistema FGF/FGFR desempenha papéis importantes em inúmeros processos tais como migração, diferenciação, sobrevivência e proliferação celulares, sendo um relevante agente pro-angiogênico que contribui para o desenvolvimento e progressão de uma variedade de condições fisiológicas e patológicas. No que se refere ao câncer, a angiogênese favorece a proliferação das células tumorais, invasão local e metástase hematogênica. A possibilidade de modular a angiogênese alterando o equilíbrio entre o balanço pró e anti-antiangiogênico tem, portanto, grande potencial terapêutico. Neste sentido, são relevantes as pesquisas buscando a identificação e caracterização funcional de moléculas, como PTX3, que é um antagonista natural do sistema FGF/FGFR. O objetivo deste estudo foi caracterizar a expressão de PTX3 em linhagens humanas derivadas de sarcoma (HT 1080, SAOS 2), cólon (HCT 116, CACO 2 e SW 480) e melanoma (SK-MEL 37 e SK-MEL 188) bem como avaliar o seu efeito sobre a proliferação celular e perfil de expressão de genes relacionados à resposta inflamatória e angiogênese nestas células. A expressão gênica foi avaliada por RT-PCR e a proliferação celular analisada pelo método MTT e por contagem de células coradas pelo Azul de Tripan. Os aspectos relacionados à morfologia foram investigados por microscopia de contraste de fase e por imunofluorescência utilizando faloidina-rodamina conjugada com TRITC para identificação da estrutura de actina-F nas células. As linhagens tumorais HT 1080, HCT 116, SK-MEL 37 e SK-MEL 188 apresentaram expressão basal tanto de FGF 2 quanto de todos os receptores para FGF (FGFR 1-4) investigados. Nenhuma das linhagens apresentou expressão basal de FGF8. Níveis basais de PTX3 foram detectados nas células HT 1080, HCT 116, SW 480 e SK-MEL 188. Resultados preliminares indicaram que PTX3 parece interferir negativamente na proliferação da linhagem de fibrosarcoma humano HT 1080. Os resultados obtidos através da análise, por imunofluorescência, sugerem que PTX3 promove alterações no citoesqueleto das células HT 1080 e HCT 116. Nas primeiras, uma aparente diminuição da abundância de filopódios foi detectada, e nas últimas, parece haver uma diminuição no número de filamentos transcelulares. Esses resultados preliminares suscitam a necessidade de aprofundamento dos estudos buscando a elucidação do papel de PTX3 nos mecanismos relacionados à migração e à proliferação celular dependentes de FGF em células tumorais humanas bem como a avaliação do potencial terapêutico de PTX3 como agente anti-angiogênico.
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Vietta, Giovanna Grünewald. "Caracterização dos níveis da pentraxina-3 (PTX-3) em amostra de pacientes com cardiopatia isquêmica estável na população brasileira." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2008. http://hdl.handle.net/10183/17435.
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Introdução: A Pentraxina-3 (PTX-3), produzida principalmente por macrófagos e células da vasculatura endotelial em resposta aos primeiros sinais pró-inflamatórios, tem sido apontada como um novo marcador de eventos coronarianos. Este estudo objetiva caracterizar os níveis plasmáticos de PTX-3 em pacientes com doença arterial coronariana estável em uma população brasileira, bem como sua relação com outros marcadores de risco cardiovascular e manifestação clínica de doença arterial coronariana (DAC). Métodos: Caracterização dos fatores de risco cardiovascular clássicos, e determinação dos níveis plasmáticos de PTX-3, proteína C reativa ultra-sensível (PCRus), interleucinas 18 (IL-18) e 10 (IL-10) foram realizadas numa coorte de 132 pacientes com doença arterial coronariana documentada, estáveis clinicamente. A determinação dos níveis plasmáticos de PTX-3, PCRus, IL-18 e IL-10 foi realizada pela técnica de ELISA utilizando-se kits comercialmente disponíveis. Os resultados dos valores dos marcadores inflamatórios foram comparados entre participantes que tiveram eventos clínicos ou não durante o seguimento médio de 47 meses. Resultados: Os níveis de PTX-3 e PCR-us coletados na primeira e segunda amostra foram semelhantes 3,45 e 3,84 ng/mL, e 4,89 e 4,72 mg/dL, respectivamente. A correlação de Pearson entre a primeira e segunda amostra foi maior para a dosagem de PCR-us que para o PTX3 (r=0,603 e r=0,356; p<0,001). Os níveis médios de PTX-3 em pacientes sem eventos foram 3,49±1,94ng/mL e nos pacientes que desenvolveram eventos 3,48±2,33ng/mL (p= 0,982). Para PCR, os valores foram de 5,07±8,26mg/mL e 4,60±4,66mg/dL (p= 0,737), respectivamente. Não foi encontrada associação entre níveis de PTX-3 e fatores de risco cardiovascular. Valores de PCRus foram associados com níveis séricos de LDL e a fração de ejeção do ventrículo esquerdo, não havendo relação com outros fatores de risco. Conclusões: Nesta amostra de indivíduos com DAC estável os níveis de PTX- 3 e PCR foram mais elevados do que em outras populações. Não identificamos fatores de risco relacionados com níveis aumentados de PTX-3 ou sua relação com eventos em médio prazo.
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Marschner, Julian [Verfasser], and Hans-Joachim [Akademischer Betreuer] Anders. "Die Rolle von Pentraxin 3 bei entzündlichen Nierenerkrankungen / Julian Marschner ; Betreuer: Hans-Joachim Anders." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1193048931/34.
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Gifoni, Markus Andret Cavalcante. "Envolvimento da pentraxina 3 (PTX3) na patogênese da cistite hemorrágica induzida por ifosfamida em camundongos." reponame:Repositório Institucional da UFC, 2008. http://www.repositorio.ufc.br/handle/riufc/2592.
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GIFONI, Markus Andret Cavalcante. Envolvimento da pentraxina 3 (PTX3) na patogênese da cistite hemorrágica induzida por ifosfamida em camundongos. 130 f. 2008. Dissertação (Mestrado em Farmacologia) - Universidade Federal do Ceará. Faculdade de Medicina, Fortaleza, 2008.Submitted by denise santos (denise.santos@ufc.br) on 2012-05-04T16:36:22Z No. of bitstreams: 1 2008_dis_macgifoni.pdf: 3631477 bytes, checksum: 2a13693f0c54b428c60eea4f01db4b4f (MD5)
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The Hemorrhagic Cystitis (HC) is an inflammatory reaction usually associated with Cancer Chemotherapy with Oxazaphosphorines. It is an innate inflammatory response to vesical irritation by Acrolein, an hepatic metabolite of the treatment with Iphosphamide and Cyclophosphamide. The role of toll-like receptor (TLR) engagement and TNF-α and IL-1β expression and the involvement of iNOS and COX-2 in the pathogenesis has been well demonstrated in a murine model of HC. Recent data configure pentraxin 3 (PTX3) as an inflammatory mediator in several experimental models of innate immune response in vivo, with a straight relation with TLR engagement. Because of that, this study looks at the involvement of PTX3 in the pathogenesis of iphosphamide–induced HC in mice. For this purpose, the mRNA to PTX3 and IL-1β t was quantified by RT-PCR in groups of C57BL6 mice treated with Iphosphamide or Saline. After that, groups of transgenic and Knock-Out mice to PTX3 and its respectives wild-type controls were treated with Iphosphamide or saline with intention to measure the Bladder Wet Weight (BWW), histomorphometric scores and Immunohistochemistry and RT-PCR to PTX3, IL-1β, TNF-α e iNOS analysis. The transgenic mice and its controls were killed in 3h and 12h after the treatment, while the PTX3 KO and its controls were killed after 12 hours. Finally, the experimental HC was modulated by pretreatment with Talidomide, Pentoxiphiline, MESNA, Amifostine and Aminoguanidine and the bladders submitted to immunohistochemistry assay (PTX3, TNF-α, IL-1β and iNOS). By RT-PCR quantification, mRNA for PTX3 was expressed 70 times more in mice treated with iphosphamide than in controls, while IL-1β RNAm had an expression rate of 10 times. PTX3 transgenic mice had initial reduction of the inflammatory response with less expression of PTX3 and TNF-α and greater expression of iNOS. In the other hand, after 12 hours, the PTX3 transgenic mice had more inflammatory signs with superior expression of all the mediators. There was no difference between the PTX3 KO mice and its controls in the HC intensity although differences between groups were seen in cytokines expression. Talidomide and MESNA produced substantial reduction on the PTX3 expression, the same was seen to TNF-α, while the amifostine marked inhibition of HC had low effect on PTX3 expression. These data as a whole, point to an unequivocal involvement of PTX3 in the pathogenesis of innate inflammatory response of HC in mice with close relation with TNF-α engagement.
A cistite hemorrágica (CH) é um fenômeno inflamatório frequentemente associado à quimioterapia com oxazafosforinas. Trata-se de uma resposta inflamatória inata à ação da Acroleína (ACR), metabólito hepático comum à Ifosfamida (IFO) e à ciclofosfamida (CTX). O papel da resposta ao recrutamento de receptores toll-like (TLR) e do estímulo por TNF-α e IL-1β com envolvimentto de iNOS e COX-2 tem sido demonstrado neste fenômeno. Estudos recentes demonstram que a Pentraxina 3 (PTX3) assume papel de mediador inflamatório em modelos de resposta inflamatória inata in vivo, sobretudo relacionada ao recrutamento de TLR. Desta forma, o presente estudo pretende investigar o possível envolvimento de PTX3 na patogênese da CH induzida por ifosfamida em camundongos. Para isso, foi realizada quantificação de RNAm por RT-PCR para PTX3 e IL-1β em camundongos C57/ BL6 tratados com ifosfamida e salina. Em seguida, o modelo experimental da CH induzida por ifosfamida foi reproduzido em grupos de camundongos com hiperexpressão e nocauteados para PTX3 em comparação com os respectivos controles do tipo selvagem e com grupos controle tratados com salina para posterior obtenção dos pesos vesicais úmidos (PVU), realização de análise histomorfométrica, imunohistoquímica e quantificação de RNAm por RT-PCR para PTX3, IL-1β, TNF-α e iNOS. Os animais transgênicos e seus controles foram sacrificados com tempos de 3h e 12h após o tratamento, enquanto os nocauteados e seus controles foram sacrificados com 12 horas do tratamento. Finalmente, a CH em animais C57/ BL6 foi modulada com o pré-tratamento com Talidomida, Pentoxifilina, MESNA, Amifostina e Aminoguanidina para a posterior marcação imunohistoquímica com PTX3, IL-1β, TNF-α e iNOS. Observou-se que o RNAm de PTX3 está cerca de 70 vezes mais expresso em animais com CH, contra uma razão de expressão de 10 para IL-1β. Animais trangênicos para PTX3 têm redução inicial da resposta inflamatória com expressão inferior de PTX3 e TNF-α e expressão aumentada de iNOS e intensificação da inflamação ao tempo de 12 horas, com expressão superior dos mediadores. Não houve diferenças significativas de intensidade da CH em animais KO em relação aos controles. A modulação da CH por talidomida e MESNA produziu redução importante sobre a expressão de PTX3, enquanto a inibição da CH por amifostina não teve redução expressiva da pentraxina. Em conjunto, estes dados apontam para um envolvimento inequívoco de PTX3 na fisiopatologia da inflamação inata em modelo de CH murino com íntima relação coma expressão de TNF-α.
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Becker, Christopher A. [Verfasser]. "Die Rolle von Pentraxin 3 und Interleukin-6-Transsignaling im Rahmen des Polytraumas / Christopher A. Becker." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2015. http://d-nb.info/1079524711/34.
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Flatscher, Katharina [Verfasser], and Katrin [Akademischer Betreuer] Karl. "Stellenwert von Pentraxin-3 als diagnostischer Marker für die Prädiktion der Präeklampsie / Katharina Flatscher. Betreuer: Katrin Karl." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1053913710/34.
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Gullo, Jackson da Silva. "Associação entre os níveis séricos de pentraxina 3 e a mortalidade de pacientes vítimas de traumatismo crânio-encefálico grave." reponame:Repositório Institucional da UFSC, 2013. http://repositorio.ufsc.br/handle/123456789/103292.
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Dissertação (mestrado) - Universidade Federal de Santa Catarina, Centro de Ciências da Saúde, Programa de Pós-Graduação em Ciências Médicas, Florianópolis, 2010Made available in DSpace on 2013-07-16T04:02:21Z (GMT). No. of bitstreams: 1 276711.pdf: 1258846 bytes, checksum: 74a809fae7fb12b98d0bba9fc2970e03 (MD5)
Introdução: O trauma cranioencefálico (TCE), é a umas das maiores causas de morbidade e mortalidade no mundo. Pentraxina 3 (PTX3) é um componente do sistema humoral de resposta imune inata que tem sido estudada como marcador para inflamação, infecções ou patologias cardiovasculares. Objetivos: Investigar a associação entre os níveis séricos de PTX3 e a mortalidade de pacientes com TCE grave. Métodos: A associação independente entre os níveis séricos de PTX3 após o TCE grave (Escala de Coma de Glasgow, ECG ? 8) e a mortalidade no momento da alta foi analisada em um estudo prospectivo de 83 pacientes consecutivos, por uma análise de regressão logística múltipla. Resultados: A média de idade dos pacientes foi de 35 anos e 85 porcento são homens. Os níveis séricos de PTX3 são determinados em 18.0 (DP ± 17.0) horas após o trauma. Pacientes que morreram apresentaram uma média no nível sérico de PTX3 de 9,95 ?gm / ml (DP ± 6,42) em comparação com 5,46 ?gm / ml (DP ± 4,87) no Grupo de sobreviventes (p = 0,007). Após a análise por regressão logística múltipla, níveis séricos de PTX3 maior que 10 ?gm/ml foi 3 vezes mais associado com à morte do que os níveis mais baixos (OR ajustado 3.38, IC 95% 1.10 - 10.45, p = 0.03). A idade avançada, anormalidades pupilares e menor pontuação na ECG também foram associadas independentemente à mortalidade. Conclusão: Níveis séricos de PTX3 após o TCE grave estão associados à maior mortalidade no momento da alta. Nossa descoberta sugere que PTX3 pode ser um marcador útil de TCE grave e seu prognóstico.
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Slusher, Aaron L. "COUNTERREGULATORY EFFECTS OF PTX3 ON INFLAMMATION AND CELLULAR AGING." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5287.
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Pentraxin 3 (PTX3) is a vital regulator of innate immune function that has been shown to counterregulate pro-inflammatory signaling and protect against the development of cardiovascular disease (CVD). Less is known about how PTX3 may mitigate against CVD risk by regulating the pro-inflammatory response at the cellular level. Therefore, this dissertation details four manuscripts which aimed to examine the capacity of PTX3 to regulate the innate immune response of peripheral blood mononuclear cells (PBMCs) isolated from healthy adults. Manuscript 1 examined the capacity of PTX3 to alter the inflammatory milieu following in vitro stimulation of isolated PBMCs with the pro-inflammatory lipid palmitate. In addition, Manuscript 2 sought to examine how participation in acute exercise, a powerful anti-inflammatory behavior that reduces CVD risk, alters the inflammatory phenotype and response of mononuclear cells following ex vivo stimulation with lipopolysaccharide (LPS). Manuscript 3 aimed to further elucidate the potential impact of cardiorespiratory fitness on the capacity of PTX3 to stimulate an innate immune response prior to and immediately following acute exercise in aerobically trained and untrained individuals. Finally, Manuscript 4 investigated the impact of healthy aging on plasma PTX3 concentrations and its relationship with telomere length in middle-aged compared to young adults. The capacity of isolated PBMCs to express a key cellular mechanism involved in maintaining longer telomere lengths, human telomerase reverse transcriptase (hTERT), following cellular stimulation with LPS, PTX3, and PTX3+LPS was also examined to address a mechanism that might explain how persistent exposure of circulating immune cells to the age-related pro-inflammatory milieu contributes to the shortening of telomere lengths.
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Böhme, Michael Hjalmar Axel [Verfasser]. "Assoziationen von Pentraxin 3 und anderen inflammatorischen Markern mit Restnierenfunktion, Nierenersatztherapiedauer und kardiovaskulären Erkrankungen bei Dialysepatienten / Michael Hjalmar Axel Böhme." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2011. http://d-nb.info/1025354389/34.
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Martin, Laura Fernandes [UNESP]. "Expressão de Pentraxina 3 no líquido amniótico e imunolocalização nas membranas corioamníóticas de gestações de termo e complicadas por parto pré-termo." Universidade Estadual Paulista (UNESP), 2013. http://hdl.handle.net/11449/108487.
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000747189.pdf: 1571276 bytes, checksum: cb0e6f84e4a758217e41fa9ef75dba98 (MD5)Changes in the Pentraxin 3 (PTX3) expression throughout pregnancy are not well established but in pregnancy complications higher expression have been described. To evaluate expression of PTX3 in amniotic fluid (AF) throughout the last weeks of normal pregnancies and in pregnancies complicated by preterm delivery (PTD). A crosssectional study was conducted with 120 pregnant women in term and PTD. Samples of AF from all patients were obtained during cesarean section. Amniochorion membranes were collected to localization of PTX3 using immunohistochemistry. Regarding term pregnancies, PTX3 expression increased slightly throughout weeks, but these expressions are not statistically different. Among preterm pregnancies, those with preterm labor (PL) had a higher PTX3 levels than those not in labor and there was a risk increased of 1% in the occurrence of PL when there was a rise of 1 pg/mL of PTX3. Amniotic epithelial, chorionic and decidual cells presented immunoexpression of PTX3. PTX3 is a physiologic constituent of the AF, and its expression is elevated in the presence of spontaneous PL suggesting that PTX3 play a role in the innate immune response during the gestational complications that are related with an infectious/inflammatory conditions. The amniochorion membranes are sources of PTX3
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Martin, Laura Fernandes. "Expressão de Pentraxina 3 no líquido amniótico e imunolocalização nas membranas corioamníóticas de gestações de termo e complicadas por parto pré-termo /." Botucatu, 2013. http://hdl.handle.net/11449/108487.
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Orientador: Márcia Guimarães da SilvaCoorientador: Rodrigo Paupério Soares de Camargo
Banca: Gisele Alborghetti Nai
Banca: Denise Fecchio
Resumo: Não disponível
Abstract: Changes in the Pentraxin 3 (PTX3) expression throughout pregnancy are not well established but in pregnancy complications higher expression have been described. To evaluate expression of PTX3 in amniotic fluid (AF) throughout the last weeks of normal pregnancies and in pregnancies complicated by preterm delivery (PTD). A crosssectional study was conducted with 120 pregnant women in term and PTD. Samples of AF from all patients were obtained during cesarean section. Amniochorion membranes were collected to localization of PTX3 using immunohistochemistry. Regarding term pregnancies, PTX3 expression increased slightly throughout weeks, but these expressions are not statistically different. Among preterm pregnancies, those with preterm labor (PL) had a higher PTX3 levels than those not in labor and there was a risk increased of 1% in the occurrence of PL when there was a rise of 1 pg/mL of PTX3. Amniotic epithelial, chorionic and decidual cells presented immunoexpression of PTX3. PTX3 is a physiologic constituent of the AF, and its expression is elevated in the presence of spontaneous PL suggesting that PTX3 play a role in the innate immune response during the gestational complications that are related with an infectious/inflammatory conditions. The amniochorion membranes are sources of PTX3
Mestre
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Göbel, Jens [Verfasser], Giuliano [Akademischer Betreuer] Ramadori, Michael [Akademischer Betreuer] Oellerich, and Thomas [Akademischer Betreuer] Lorf. "Bestimmung von Pentraxin-3 im Blutserum und dessen Bedeutung für Lebererkrankungen / Jens Göbel. Gutachter: Giuliano Ramadori ; Michael Oellerich ; Thomas Lorf. Betreuer: Giuliano Ramadori." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2013. http://d-nb.info/1044173262/34.
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Palm, Maria. "Oxidative Stress, Angiogenesis and Inflammation in Normal Pregnancy and Postpartum." Doctoral thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-171165.
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The aims were to investigate oxidative stress (I), angiogenesis (II) and inflammation (III-IV) in healthy women during pregnancy and postpartum. Oxidative stress was estimated by measurement of 8-iso-PGF2α and the antioxidants α- and γ-tocopherol. The angiogenic factors PlGF, VEGF-A and the antiangiogenic factor sFlt1 were measured to estimate angiogenesis. PTX3, IL-6, TNF-α and a PGF2α metabolite were measured to estimate inflammation. Out of 52 included women, 15 had minor pregnancy complications and 37 were classified as normal. In study III data from all 52 women were used. For the other studies (I, II and IV) only data from the 37 women with normal pregnancy were used. Pregnancy was associated with increased levels of 8-iso-PGF2α with advancing gestational age. The median postpartum value corresponded to values observed in early gestation and a significant decrease was observed from late pregnancy to postpartum. Lipid-adjusted α- and γ-tocopherol levels decreased with advancing gestational age (I). PlGF increased from early pregnancy until weeks 29–30 and thereafter decreased until week 40. sFlt1 levels were relatively constant until weeks 29–30, when they increased, reaching a peak at weeks 39–40. Postpartum levels were low. The sFlt1:PlGF ratio decreased from weeks 9–12, was constantly low from weeks 19–20 to 37–38 and then increased to weeks 39–40. VEGF-A was detectable in only 8 % of the samples during pregnancy and in 64 % postpartum (II). There was a continuous increase of PTX3 as pregnancy progressed. The increase was most evident after week 31 with the highest levels just before delivery (III). IL-6 increased throughout pregnancy and remained high postpartum. No change in TNF-α could be seen with advancing gestational age or postpartum. The PGF2α metabolite levels increased throughout pregnancy and decreased postpartum (IV). In conclusion, normal pregnancy is associated with mild oxidative stress and inflammation. This might have physiological effects for normal pregnancy development. By delineating how these mediators of oxidative stress, angiogenesis and inflammation fluctuate throughout normal pregnancy and postpartum, we have established a reference for studies of these factors in pregnancy complications.
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Yenuga, Hima Priya. "Characterization of proteins found in serum and sputum samples from ventilator associated pneumonia patients." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1590233445157576.
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"Pentraxin 3 in the lung and neutrophils." Thesis, 2013. http://hdl.handle.net/10388/ETD-2013-08-1195.
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Respiratory diseases are a major cause of human morbidity and mortality and are a leading cause of economic loss to livestock producers. The respiratory tract is constantly in contact with dust, bacteria, fungi, viruses and other pathogenic agents that are found in the air. Normally, the body has the ability to clear these foreign particles. However, physiological and environmental stresses can impair airway defense mechanisms resulting in establishment of pulmonary infections. The microbes and their products engage various receptors in the lung to activate epithelium, endothelium, macrophages, neutrophils and other cells. The activation of inflammatory cascade in the lung results in recruitment of neutrophils, damage to air-blood barrier and development of edema. Although there have been significant advances in our understanding of mechanisms of lung inflammation, there have been a lack of any significant advances in the development of new therapeutics to manage lung disease, which may suggest that our understanding of the inflammatory mechanisms is still incomplete.
Pentraxin 3 (PTX3) is an innate immune protein which has been implicated in a diverse range of inflammatory processes, such as recruitment of cells and production of cytokines. PTX3 is an acute phase protein, with low or undetectable levels in the circulation of healthy humans and animals, and rapid, dramatic increase in inflammatory diseases. The expression and function of this protein has not been characterized in the lungs of domestic animal species. Because of potential implications of PTX3 in lung inflammation, I studied the expression of PTX3 in normal and inflamed lungs of calves, pigs, horses, foals and humans. Lungs from all of these species showed expression of PTX3 in airway epithelium, alveolar septa, vascular endothelium and inflammatory cells. Western blot performed on homogenates from normal and inflamed lungs from calves and pigs show an increased expression of PTX3 in inflamed lungs (P<0.05).
Because protein function is influenced by its location in the cell, I clarified the subcellular expression of PTX3 with immuno-electron microscopy on normal and inflamed calf and horse lungs. PTX3 was localized on pulmonary intravascular macrophages, monocytes, neutrophils and, unexpectedly, platelets. PTX3 was also present in the nuclei of neutrophils, monocytes and pulmonary intravascular macrophages.
Neutrophils are critical regulators of acute lung inflammation. Having observed PTX3 in neutrophils, I investigated the effect of E. coli lipopolysaccharide-induced activation on PTX3 in neutrophils in vitro. Neutrophils challenged with E. coli LPS were examined at 30, 60, 90 and 120 minutes after the treatment. Normal peripheral blood neutrophils showed PTX3 expression. Neutrophils activated with LPS appeared ruffled and showed loss of PTX3 expression at 30 minutes followed by recovery of the expression. Western blots performed on normal and activated neutrophil homogenates did not show any differences (P=0.05).
Collectively, the data show PTX3 in normal and inflamed lungs across multiple species. PTX3 was also detected in normal and activated neutrophils. While the function of intriguing localization of PTX3 in the nuclei as well as in platelets is not known, the similarity of expression across the species suggest a role for PTX3 in lung inflammation.
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Chang, Wan-Ting, and 張睆婷. "The role of Pentraxin 3 in human cervical cancer cells." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/98416951269040909154.
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碩士中山醫學大學
生化暨生物科技研究所
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Cervical carcinoma is one of the most frequent cancers in women and is associated with high-risk human papilloma virus (HPV) infection. It causes many women death in Taiwan. PTX3 also called tumor necrosis factor-inducible protein 14 gene (TSG-14) were mapped to chromosomes 24q28.3. PTX3 regulate cell growth, differentiation, invasion and apoptosis have been reported. However, its involvement in human cervical cancer progression remains unclear. In our study, Using human cervical cancer tissues array, we found that expression level of PTX3 is higher in human cervical cancer tissues than that is human normal cervical tissues. We also found that PTX3 protein expression is higher in high malignant Hela and SiHa cells than in low malignant C33A cells. To verify the biological function of PTX3 in cervical cancer cells, we constructed Lentivirus-mediated PTX3 interference and found growth retargation of cervical cancer assessed by the MTT assay. Likewise, inhibition of PTX3 expression induced cell-cycle arrest in Hela and SiHa cells by up-regulating the expression of p-cdc25c, p-cdc2, p21 and p27, down-regulating the expression of cyclin B1、cdc2 and cdc25c protein expressions. Knockdown of PTX3 decreased migration and invasion in HeLa and SiHa cells, and down-regulation of MMP-2, MMP-9 and u-PA. Our results suggest that PTX3 plays an important role in regulation of proliferation and invasion of human cervical cancer, and it can be a valuable marker in detecticy cervical cancer progression. Therefore, PTX3 is a master regulator of human cervical growth, being an useful in easlier predicting target for cervical cancer prognosis.
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Göbel, Jens. "Bestimmung von Pentraxin-3 im Blutserum und dessen Bedeutung für Lebererkrankungen." Doctoral thesis, 2013. http://hdl.handle.net/11858/00-1735-0000-000E-0135-C.
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Aufgabe dieser Arbeit war es, den Serumspiegel von Pentraxin-3-Werten im Blutplasma bei Lebererkrankungen zu bestimmen und mit anderen diagnostischen Parametern zu vergleichen. Vorausgegangene Studien hatten bereits darauf hingewiesen, dass PTX3-Werte als früh verfügbare und aussagekräftige Marker bei Entzündungskrankheiten in verschiedenen Organen hilfreich sein können.
Es wurden zwei Patientenkollektive miteinander verglichen. Von 25 Patienten ohne Lebertransplantation und von 39 Patienten nach Lebertransplantation wurden die PTX3-Werte mit Hilfe des „Quantikine® Human Pentraxin 3/TSG-14 Immunoassay“ gemessen. Die Werte der Patienten nach Lebertransplantation wurden noch unterteilt in die Zeiträume drei oder mehr Monate sowie fünf oder mehr Monate nach der Transplantation.
Die statistische Prüfung erfolgte mit Hilfe des t-Tests. Das Patientenkollektiv mit Lebererkrankungen wies hochsignifikante Steigerungen des PTX3-Wertes gegenüber dem Normwert auf. Das jeweilige Patientenalter sowie das Geschlecht der untersuchten Personen besaßen nur einen geringfügigen Einfluss auf die PTX3-Konzentration. Bei Patienten mit Lebertransplantation hatten sich die PTX3-Werte nach drei oder mehr Monaten weitgehend normalisiert, weitere Messungen nach fünf oder mehr Monaten bestätigten diese Tendenz, die geringfügige Differenz zum Normwert war nicht mehr statistisch signifikant.
Die PTX3-Messwerte der an Lebererkrankungen leidenden Patienten wurden zudem mit anderen klinisch-diagnostischen Parametern verglichen. Im Vergleich mit CRP, ALT, AST, AP und GGT zeigte die statistische Analyse signifikante und hochsignifikante Unterschiede mit stärkeren Erhöhungen der PTX3-Werte. Daraus lässt sich ableiten, dass PTX3 eine zuverlässige Rolle bei der klinischen Diagnose von Lebererkrankungen einnehmen kann.
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Chih-Chia and 張秩嘉. "Study of plasma Pentraxin 3 in patients with pelvic inflammatory disease." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/86414237513515508546.
Full textAbstract:
博士中山醫學大學
醫學研究所
99
Pentraxin 3 (PTX3) plays an important role in innate immune responses and in inflammation disease. The aim of this study was to investigate the diagnostic and prognostic potential of PTX3 in pelvic inflammatory disease (PID) and correlate it with the severity and outcome of PID. In this study, we collected blood specimens from 64 patients with PID before and after treatment and 70 healthy controls and measured the plasma levels of PTX3 using enzyme-linked immunosorbent assay (ELISA) kits. We found that the plasma level of PTX3 expression was elevated in PID patients compared with healthy controls, and decreased significantly after they received treatment. When we set the cutoff level of plasma PTX3 at 2.87 ng/mL, PTX3 had higher sensitivity (84.38 %) and lower false negative rate (15.63 %) than CRP (79.69 % and 20.31 %, respectively) in predicting PID. The level of PTX3 also exhibited a significant correlation with length of hospital stay (r=0.581, p<0.001). Plasma PTX3 concentration not only predicts the presence of PID with lower false negative rate than CRP, but plasma PTX3 concentration is also affiliated with the length of the hospital stay.
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Holubcová, Zdeňka. "Dlouhý pentraxin 3 - prediktivní biomarker poškozující zánětové odpovědi u nemocných operovaných na srdci?" Doctoral thesis, 2017. http://www.nusl.cz/ntk/nusl-352799.
Full textAbstract:
(LONG PENTRAXIN 3 - A PUTATIVE BIOMARKER WITH PREDICTIVE VALUE TO IDENTIFY THE ADVERSE INFLAMMATORY RESPONSE IN CARDIAC SURGICAL PATIENTS?) INTRODUCTION. Cardiac surgery is well established for development of systemic inflammatory response. There are still no biomarkers with significant predictive value to identify patients at risk. AIM. The aim of this study was to compare the dynamics of pentraxin 3 (PTX3) and other inflammatory biomarkers (CRP, TLR2 and IL-8) after cardiac surgery with particular regards to different postoperative clinical manifestation of inflammatory response. Furthermore to evaluate the association between perioperative inflammatory biomarkers (PTX3, CRP, IL-8, IL-18, IL-18BP, TLR2, MMP7, MMP8, sFas a sFasL) and atrial fibrillation (AF) in cardiosurgical patients. METHODS. Forty-two patients undergoing open heart surgery with the use of cardiopulmonary bypass were included in the study and divided in 2 groups according to the extent of clinical manifestation of inflammatory response: Group A (n = 21) - patients with different severity of systemic inflammatory response syndrome (SIRS) and Group B (n = 21) - patients with uneventful postoperative period (no SIRS). The same group of 42 patient were divided in 3 groups according to occurrence of atrial fibrillation (AF): Group A...
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Hung, Tung-Wei, and 洪東衛. "Pentraxin 3 Activates JNK Signaling and Regulates the Epithelial-To-Mesenchymal Transition in Renal Fibrosis." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/3d5rx5.
Full textAbstract:
博士中山醫學大學
醫學研究所
106
Objective：Tubulointerstitial fibrosis can lead to end-stage renal disease. Pentraxin 3 (PTX3) is an acute phase protein produced by resident and innate immunity cells. We investigated the effect of PTX3 on cultured human proximal tubular epithelial (HK-2) cells and a rat unilateral ureteral obstruction (UUO) model of renal fibrosis. Methods and Materials：Gain-of-function experiments were used to examine the effect of recombinant human PTX3 (Rh-PTX3) on HK-2 cells. Cell proliferation (MTT assay) and in vitro cell migration were measured. The levels of PTX3, p-JNK1/2, and EMT markers were measured using immunohistochemistry, RT-PCR, and western blotting in UUO rats and HK-2 cells. Results：HK-2 cells treated with Rh PTX3 did not affect cell viability, but significantly increased cell migration. Moreover, Rh-PTX3 increased the expression of snail, slug, N-cadherin, and vimentin, decreased the expression of E-cadherin, and increased the phosphorylation of JNK1/2. SP600126 (a specific JNK1/2 inhibitor) enhanced the effects of Rh-PTX3. Rats with UUO exhibited time-dependent increased levels of PTX3, p-JNK1/2, and vimentin, and decreased expression of E-cadherin. Conclusion and Suggestion：Our results suggest that PTX3 induces cell migration via upregulation of EMT in a JNK1/2-dependent mechanism, and highlight the role of PTX3 in the pathogenesis renal fibrosis.
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Mendes, Maria Silvina Marques. "Human fluids pretreatment using three-phase partitioning systems for the diagnosis and prognosis of lung cancer." Master's thesis, 2021. http://hdl.handle.net/10773/31941.
Full textAbstract:
Lung cancer is responsible for the highest rate of cancer mortality worldwide. The 5-year survival rate of lung cancer is less than 15%, mainly because most lung cancer patients are diagnosed at late stages. Therefore, early detection of lung cancer represents one of the most effective approaches to help reduce the high associated mortality and morbidity. Technological advances in genomics and proteomics fields have disclosed many novel cancer biomarkers, which can be used in early cancer detection. Pentraxin-3 is one of these promising biomarkers, found in serum, for lung cancer diagnosis and prognosis. However, human serum is a complex matrix whose protein profile mainly comprises human serum albumin (HSA) and immunoglobulin G (IgG). These proteins can interfere or even mask the detection and quantification of less abundant ones, such as PTX3, leading to false results. To contribute towards an earlier and more reliable diagnosis of lung cancer, there is a need to implement sample pretreatment steps that permit the depletion of the most abundant proteins and the concentration of tumor biomarkers of interest. In this context, three-phase partitioning (TPP) based on aqueous biphasic systems (ABS) are an alternative to conventional pretreatment techniques that use expensive affinity resins or volatile organic solvents.
The main goal of this work is to develop new TPP systems based on ABS composed of polymers/copolymers and salts as alternative serum pretreatment strategies. To this end, novel TPP-ABS formed by the homopolymers PPG 400, PEG 400, PEG 600, PEG 1000 and PEG 2000, and the copolymers Pluronic PE6200, Pluronic PE6400, Pluronic L35 and UCON, and a citrate buffered salt, were investigated in terms of their performance to simultaneous deplete HSA and IgG and extract the biomarker PTX-3 to the polymer-rich phase. According to the results obtained, TPP systems formed by PPG 400, PEG 1000, PEG 2000 and UCON allow depletion efficiencies above 80% for both proteins, with the systems formed by PEG 1000 and UCON allowing depletions efficiencies reaching 100% for both abundant proteins. Among the best studied systems, only the TPP system formed by PEG 1000 allows the complete extraction of PTX-3 towards the polymer-rich phase, while keeping the complete depletion of IgG and HSA. ELISA assays demonstrate the better performance of this TPP foe the PTX-3 quantification in the pretreated human serum samples, thus representing a promising alternative for the pretreatment of human serum for the diagnosis and prognosis of lung cancer.A nível mundial, o cancro do pulmão apresenta a maior taxa de mortalidade associada a doenças oncológicas. A taxa de sobrevivência a 5 anos deste tipo de tumor é inferior a 15%, devido ao facto da maioria dos pacientes serem diagnosticados em fases avançadas. Assim, a deteção precoce do cancro do pulmão representa uma das abordagens mais promissoras para a redução da sua elevada mortalidade e morbidade. Os avanços tecnológicos nas áreas da genómica e da proteómica permitiram identificar novos biomarcadores que podem ser utilizados na deteção precoce de tumores. A pentraxina-3 (PTX3) é um destes biomarcadores, uma vez que a sua deteção e quantificação no soro humano permite o diagnóstico e prognóstico de cancro do pulmão. Porém, o soro humano é uma matriz muito complexa e cujo conteúdo proteico é constituído principalmente por albumina do soro humano (ASH) e imunoglobulina G (IgG). Estas proteínas podem interferir ou mesmo mascarar a deteção e quantificação de proteínas menos abundantes, tais como a PTX3, conduzindo a resultados falsos. De modo a possibilitar um diagnóstico precoce e mais fidedigno do cancro do pulmão, é necessário implementar etapas de pré-tratamento do soro humano que permitam a depleção das proteínas mais abundantes e simultânea concentração de biomarcadores tumorais. Neste contexto, os sistemas de partição em três fases à base de sistemas bifásicos aquosos (SAB) surgem como uma técnica alternativa às técnicas de pré-tratamento atuais que usam resinas de afinidade dispendiosas ou solventes orgânicos voláteis. O objetivo principal deste trabalho é desenvolver novos sistemas de partição em três fases com base em SAB constituídos por polímeros/copolímeros e sais como estratégias alternativas de pré-tratamento de soro humano. Para tal, foram estudados novos sistemas compostos pelos homopolímeros PPG 400 e PEGs 400, 600, 1000 e 2000, e pelos copolímeros Pluronic PE6200, PE6400 e L35, e UCON, e tampão citrato, em termos da sua capacidade para simultaneamente precipitar a ASH e IgG na interfase e extrair o biomarcador PTX-3 para a fase rica em polímero. De acordo com os resultados obtidos, os sistemas formados por PPG 400, PEG 1000, PEG 2000 e UCON permitiram eficiências de depleção acima de 80% para ambas as proteínas, com os sistemas formados por PEG 1000 atingindo percentagens de depleção de 100% para as proteínas mais abundantes. Entre os melhores sistemas estudados, apenas o sistema com PEG 1000 permitiu a extração total da PTX-3 na fase rica em polímero, mantendo a depleção completa da IgG e HSA. Os ensaios de ELISA realizados mostraram a capacidade melhorada deste sistema para a quantificação de PTX-3 em amostras pré-tratadas, representando uma alternativa promissora para o pré-tratamento do soro humano no diagnóstico e prognóstico do cancro do pulmão.
Mestrado em Bioquímica
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Yang-MingLiu and 劉揚民. "Purification and Crystallization Studies of Transcription Factor CCAAT/Enhancer Binding Protein delta and Inflammatory Factor Long Pentraxin 3." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/93061943844711154657.
Full textAbstract:
碩士國立成功大學
生物資訊與訊息傳遞研究所
102
Abstract Part A: CEBPδ Transcription factor CEBPδ is involved in cell differentiation, motility, growth arrest, proliferation, and cell death. Studies also suggested that CEBPδ functions differed depending on cell type and cellular context. CEBPδ has been proved as a tumor suppressor in some cancers, for example, in breast cancer. But CEBPδ also help glioblastoma cell’s survival by inflammation response and induce metastasis. Previous studies had reported CEBPδ has many posttranslational modification sites and need to form a dimer with other family member or different proteins for its function. But the detailed mechanism and function of these modifications and dimerization are still unknown. In our research we try to study and explain these mechanisms by crystallography and X-ray diffraction. So we made constructs including transactivation domain (5-186), bZip domain (190-270) and full length (5-270) of CEBPδ， and all these three proteins can be over expressed. We can’t get enough full length to crystallization because it’s poor binding affinity. Transactivation domain could be pulled down enough, but it contained nonspecific bond. Finally, we use ion exchange and gain pure protein, and screening them for potential condition of crystallization. Once optimize the potential condition it may form a crystal and provide more detail structure conformation. According to size-exclusion chromatography data, we found that CEBPδ without its bZIP domain still formed a homodimer. We supposed that besides bZIP domain, the N-terminus contributed a physical interaction to dimerization. Part B PTX3 PTX3 has been considered as an inflammatory marker, because PTX3 can recognize the extracellular pathogens and induce inflammation response for immunity. And it interacts with many cytokines within its N-terminus or C-terminus. When PTX3 deposited onto apoptotic cell, it recruited the C3 and C4 on apoptotic cell. This process presents a “eat me” signal for macrophage. But the fluid phase PTX3 would inhibit the C3 deposition for an anti-apoptotic function. Although the SAXS data of PTX3 was reported, the mechanism of these functions can’t be solved, so it need structure study to provide more information. In our study, we made construct of full length (19-381), N-terminal domain (19-182), and C-terminal CRP like domain (180-381) of PTX3. The result of expression presented that the N-terminus from bacterias was soluble the same as form eukaryotic cell, but C-terminus and full length were insoluble. By purification experiment data, we supposed that the PTX3 N-terminus form a tetramer in solution like eukaryotic PTX3, and there was degradation which we still try to remove. Although the N-terminal recombinant protein had degraded, it was stable, so we still screened this protein with degradation, and try optimization for crystal which can provide more detail information of PTX3 mechanism. The full length and C-terminus formed inclusion body. We used Guanidinium-HCl to dissolve the inclusion body and used dialysis for gaining soluble protein. But the protein production was too low to crystallization. According to size-exclusion chromatography data of protein purified by dialysis, we suppose that the C-terminus form a dimer the same as in eukaryotic cell, but full length did not form a octmer. The different between prokaryotic and eukaryotic modification system could be a reason of this result.
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Shuo-LunWu and 吳碩倫. "Transcriptional activation of pentraxin-3 gene expression is associated with EGF-induced head and neck cancer cell metastasis." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/53100809601694216208.
Full textAbstract:
碩士國立成功大學
生物資訊與訊息傳遞研究所
102
SUMMARY Overexpression of epidermal growth factor receptor (EGFR) and production of proinflammatroy cytokines are well clarified in head and neck squamous cell carcinoma (HNSCC) and correlates with invasion and metastasis. However, molecular mechanisms by which EGFR-mediated cytokines regulates metastasis of HNSCC remain unclear. Here, we identified that PTX3 is a metastasis-promoting factor that mediate EGF-induced HNSCC metastasis. Analysis of PTX3 expression between normal and malignant or metastatic tissues from HNSCC patients by using published datasets, our results indicated that expression level of PTX3 in malignant tissues was higher than in normal part in HNSCC patients. In addition, we found that EGF induced transcriptional activation of PTX3 by activating the binding of c-Jun and NF-κB factors to AP-1/NF-κB binding site of the PTX3 promoter. PI3K/AKT and NF-κB were essential for the induction of PTX3. EGF-induced PTX3 expression was significantly inhibited in c-Jun and NF-κB knockdown cells. Furthermore, we identify that NF-κB is upstream regulator to c-Jun in EGF signaling pathway. EGF stimulated the secretion of PTX3 from cancer cell, resulting in enhancing cell migration, local invasion, attachment with endothelium and distal dissemination. Effects of EGF on the induction of fibronectin and MMP9 expression, and inhibition of E-cadherin were abolished in PTX3 knockdown cells. These findings reveal the mechanism that autocrine production of EGF-induce PTX3-regulated HNSCC metastasis was through enhancing metastatic molecules, such as fibronectin and MMP9 expression. Induction of PTX3 possibly reflecting the EGFR-caused HNSCC metastasis associated with inflammation.
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Zickler, Daniel [Verfasser]. "Einfluss von C-reaktivem Protein und Pentraxin 3 auf die Kalzifikation glatter Muskelzellen und Zytokinproduktion von Monozyten im Prozess der Arteriosklerose / von Daniel Zickler." 2010. http://d-nb.info/1010399810/34.
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