Relevant bibliographies by topics / Kupffer

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Kupffer'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Kupffer"

1

Haubrich, William S. "Kupffer of Kupffer cells." Gastroenterology 127, no. 1 (July 2004): 16. http://dx.doi.org/10.1053/j.gastro.2004.05.041.

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2

Karakas, Danielle, June Li, and Heyu Ni. "Novel Mechanisms of Thrombopoietin Generation: The Essential Role of Kupffer Cells." Blood 138, Supplement 1 (November 5, 2021): 3139. http://dx.doi.org/10.1182/blood-2021-145985.

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Abstract Thrombopoietin (TPO) is the physiological regulator of hemopoietic stem cell niche and megakaryocyte differentiation, and therefore platelet production. Prevailing theory posits that TPO is constitutively expressed by hepatocytes, and levels are fine-tuned through platelet and megakaryocyte internalization/clearance via the c-Mpl receptor. Our lab has previously shown that platelet glycoprotein (GP) Ibα is indispensable for platelet-mediated TPO generation (Blood 2018), and recent reports have demonstrated that Kupffer cells, the tissue resident macrophages of the liver, contribute to the clearance of desialylated platelets. However, whether Kupffer cells may contribute to TPO generation has never been explored. To determine the possible role of Kupffer cells in TPO production, clodronate liposome was intravenously administered to deplete Kupffer cells in wild-type mice. Wild-type, Kupffer cell depleted mice showed a TPO decrease of 43.6% (±16%) 2 days post depletion, with only a gradual insignificant increase in TPO levels to day 6. Interestingly, TPO levels could not be significantly increased in wild-type Kupffer cell depleted mice even when transfused 2x10 8 wild-type or desialylated platelets, or 50mU neuraminidase. Kupffer cell depletion in IL4Rα/GPIbα-transgenic mice, which lack platelet-mediated TPO generation, showed a TPO decrease of 22.5% (±5%) from baseline 2 days post depletion, with only a gradual increase in levels to day 6, suggesting that Kupffer cells are required for constitutive in addition to platelet-mediated TPO production. As our lab has previously shown that platelet GPIbα drives platelet-mediated TPO generation, and that Kupffer cells now required, WT and GPIbα -/- platelets were co-cultured with Kupffer cells to assess interaction. Desialylated WT platelets interacted significantly more with Kupffer cells as analyzed by flow cytometry than GPIbα -/- platelets. Interestingly, desialylation of GPIbα -/- platelets did not increase binding to Kupffer cells, consolidating that desialylated GPIbα is required for Kupffer cell interaction, and subsequent TPO generation. This data demonstrates the novel and unexpected finding that Kupffer cells are required for both platelet-mediated and baseline hepatocellular TPO generation. Elucidation of the role of Kupffer cells in this crucial mechanism will provide a better understanding of why thrombocytopenias may occur in pathological states, as well as contribute to the development of TPO mimetic therapies. Disclosures No relevant conflicts of interest to declare.
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Su, Grace L., Sanna M. Goyert, Ming-Hui Fan, Alireza Aminlari, Ke Qin Gong, Richard D. Klein, Andrzej Myc, et al. "Activation of human and mouse Kupffer cells by lipopolysaccharide is mediated by CD14." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 3 (September 1, 2002): G640—G645. http://dx.doi.org/10.1152/ajpgi.00253.2001.

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Upregulation of CD14 in Kupffer cells has been implicated in the pathogenesis of several forms of liver injury, including alcoholic liver disease. However, it remains unclear whether CD14 mediates lipopolysaccharide (LPS) signaling in this specialized liver macrophage population. In this series of experiments, we determined the role of CD14 in LPS activation of Kupffer cells by using several complementary approaches. First, we isolated Kupffer cells from human livers and studied the effects of anti-CD14 antibodies on LPS activation of these cells. Kupffer cells were incubated with increasing concentrations of LPS in the presence and absence of recombinant human LPS binding protein (LBP). With increasing concentrations of LPS, human Kupffer cell tumor necrosis factor-α (TNF-α) production (a marker for Kupffer cell activation) increased in a dose-dependent manner in the presence and absence of LBP. In the presence of anti-human CD14 antibodies, the production of TNF-α was significantly diminished. Second, we compared LPS activation of Kupffer cells isolated from wild-type and CD14 knockout mice. Kupffer cells from CD14 knockout mice produced significantly less TNF-α in response to the same amount of LPS. Together, these data strongly support a critical role for CD14 in Kupffer cell responses to LPS.
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Sakai, Mashito, Ty Dale Troutman, Jason S. Seidman, Zhengyu Ouyang, Nathanael J. Spann, Yohei Abe, Kaori Ego, et al. "Deciphering liver environmental signaling pathways for Kupffer cell identity." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 187.21. http://dx.doi.org/10.4049/jimmunol.202.supp.187.21.

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Abstract Functional specialization of tissue resident macrophages occurs through environmental signals controlling activity and/or expression of transcription factors. Kupffer cells are resident macrophages in the hepatic sinusoids and have critical roles in the innate immune response and iron metabolism. Here, we characterize transcriptomic and epigenetic changes in repopulating liver macrophages following acute Kupffer cell depletion as a means to infer signaling pathways and transcription factors that promote Kupffer cell differentiation. Nr1h3 encoding LXRα is rapidly and highly induced in repopulating liver macrophages, suggesting its induction plays a crucial role in Kupffer cell differentiation. Restricted deletion of Nr1h3 in Kupffer cells reveal that it is required for shaping the Kupffer cell-specific enhancer landscape. Further, we obtain evidence that combinatorial interactions of DLL4 and TGF-β/BMP produced by sinusoidal endothelial cells and endogenous LXR ligands are required for the induction and maintenance of Kupffer cell identity. DLL4 regulation of RBPJ through Notch signaling plays a key role in activating poised enhancers to rapidly induce LXRα and other Kupffer cell lineage-determining factors. These factors in turn reprogram the repopulating liver macrophage enhancer landscape to converge on that of the original resident Kupffer cells. Using molecules which mimic these liver environment signals, we show that it is possible to induce Kupffer cell-specific genes in mouse bone marrow progenitor cells and human monocytes in vitro. Collectively, these findings provide a framework for understanding how macrophage progenitor cells acquire tissue-specific phenotypes.
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Marianneau, Philippe, Anne-Marie Steffan, Cathy Royer, Marie-Thérèse Drouet, D. Jaeck, André Kirn, and Vincent Deubel. "Infection of Primary Cultures of Human Kupffer Cells by Dengue Virus: No Viral Progeny Synthesis, but Cytokine Production Is Evident." Journal of Virology 73, no. 6 (June 1, 1999): 5201–6. http://dx.doi.org/10.1128/jvi.73.6.5201-5206.1999.

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ABSTRACT We investigated the ability of dengue virus to invade human primary Kupffer cells and to complete its life cycle. The virus effectively penetrated Kupffer cells, but the infection did not result in any viral progeny. Dengue virus-replicating Kupffer cells underwent apoptosis and were cleared by phagocytosis. Infected Kupffer cells produced soluble mediators that could intervene in dengue virus pathogenesis.
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MacPhee, P. J., E. E. Schmidt, and A. C. Groom. "Evidence for Kupffer cell migration along liver sinusoids, from high-resolution in vivo microscopy." American Journal of Physiology-Gastrointestinal and Liver Physiology 263, no. 1 (July 1, 1992): G17—G23. http://dx.doi.org/10.1152/ajpgi.1992.263.1.g17.

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Kupffer cells are generally considered fixed tissue macrophages of the liver. However, we have evidence that this opinion is incorrect. High-resolution in vivo video microscopy shows that Kupffer cells have the ability to migrate along sinusoidal walls. Images recorded from anesthetized mice show active locomotion of cells with or against the direction of blood flow or in the absence of flow. The size, changing morphology, and uptake of carbon or microspheres strongly suggest that these are Kupffer cells. Quantitative measurements were made on 29 migrating Kupffer cells. The mean speed of migration was 4.6 +/- 2.6 (SD) microns/min and was not significantly different whether migration occurred with or against the flow. When fluorescent microspheres were given in vivo as a phagocytic challenge, Kupffer cells containing few microspheres migrated more slowly (0.9 +/- 0.9 microns/min, n = 10), whereas those containing many microspheres were never seen to migrate. Individual Kupffer cells were able to move independently, i.e., in directions different from those of neighboring Kupffer cells. These findings may have major implications for the role of Kupffer cells in scavenging foreign particles and as antigen-presenting cells.
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Bilzer, Manfred, Hartmut Jaeschke, Angelika M. Vollmar, Gustav Paumgartner, and Alexander L. Gerbes. "Prevention of Kupffer cell-induced oxidant injury in rat liver by atrial natriuretic peptide." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 5 (May 1, 1999): G1137—G1144. http://dx.doi.org/10.1152/ajpgi.1999.276.5.g1137.

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The generation of reactive oxygen species (ROS) by activated Kupffer cells contributes to liver injury following liver preservation, shock, or endotoxemia. Pharmacological interventions to protect liver cells against this inflammatory response of Kupffer cells have not yet been established. Atrial natriuretic peptide (ANP) protects the liver against ischemia-reperfusion injury, suggesting a possible modulation of Kupffer cell-mediated cytotoxicity. Therefore, we investigated the mechanism of cytoprotection by ANP during Kupffer cell activation in perfused rat livers of male Sprague-Dawley rats. Activation of Kupffer cells by zymosan (150 μg/ml) resulted in considerable cell damage, as assessed by the sinusoidal release of lactate dehydrogenase and purine nucleoside phosphorylase. Cell damage was almost completely prevented by superoxide dismutase (50 U/ml) and catalase (150 U/ml), indicating ROS-related liver injury. ANP (200 nM) reduced Kupffer cell-induced injury via the guanylyl cyclase-coupled A receptor (GCA receptor) and cGMP: mRNA expression of the GCA receptor was found in hepatocytes, endothelial cells, and Kupffer cells, and the cGMP analog 8-bromo-cGMP (8-BrcGMP; 50 μM) was as potent as ANP in protecting from zymosan-induced cell damage. ANP and 8-BrcGMP significantly attenuated the prolonged increase of hepatic vascular resistance when Kupffer cell activation occurred. Furthermore, both compounds reduced oxidative cell damage following infusion of H2O2(500 μM). In contrast, superoxide anion formation of isolated Kupffer cells was not affected by ANP and only moderately reduced by 8-BrcGMP. In conclusion, ANP protects the liver against Kupffer cell-related oxidant stress. This hormonal protection is mediated via the GCA receptor and cGMP, suggesting that the cGMP receptor plays a critical role in controlling oxidative cell damage. Thus ANP signaling should be considered as a new pharmacological target for protecting liver cells against the inflammatory response of activated Kupffer cells without eliminating the vital host defense function of these cells.
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Wang, Fei, Xin Huang, Chun-Shiang Chung, Yaping Chen, Noelle A. Hutchins, and Alfred Ayala. "Contribution of programmed cell death receptor (PD)-1 to Kupffer cell dysfunction in murine polymicrobial sepsis." American Journal of Physiology-Gastrointestinal and Liver Physiology 311, no. 2 (August 1, 2016): G237—G245. http://dx.doi.org/10.1152/ajpgi.00371.2015.

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Recent studies suggest that coinhibitory receptors appear to be important in contributing sepsis-induced immunosuppression. Our laboratory reported that mice deficient in programmed cell death receptor (PD)-1 have increased bacterial clearance and improved survival in experimental sepsis induced by cecal ligation and puncture (CLP). In response to infection, the liver clears the blood of bacteria and produces cytokines. Kupffer cells, the resident macrophages in the liver, are strategically situated to perform the above functions. However, it is not known if PD-1 expression on Kupffer cells is altered by septic stimuli, let alone if PD-1 ligation contributes to the altered microbial handling seen. Here we report that PD-1 is significantly upregulated on Kupffer cells during sepsis. PD-1-deficient septic mouse Kupffer cells displayed markedly enhanced phagocytosis and restoration of the expression of major histocompatibility complex II and CD86, but reduced CD80 expression compared with septic wild-type (WT) mouse Kupffer cells. In response to ex vivo LPS stimulation, the cytokine productive capacity of Kupffer cells derived from PD-1−/− CLP mice exhibited a marked, albeit partial, restoration of the release of IL-6, IL-12, IL-1β, monocyte chemoattractant protein-1, and IL-10 compared with septic WT mouse Kupffer cells. In addition, PD-1 gene deficiency decreased LPS-induced apoptosis of septic Kupffer cells, as indicated by decreased levels of cleaved caspase-3 and reduced terminal deoxynucleotidyl transferase dUTP nick end-labeling-positive cells. Exploring the signal pathways involved, we found that, after ex vivo LPS stimulation, septic PD-1−/− mouse Kupffer cells exhibited an increased Akt phosphorylation and a reduced p38 phosphorylation compared with septic WT mouse Kupffer cells. Together, these results indicate that PD-1 appears to play an important role in regulating the development of Kupffer cell dysfunction seen in sepsis.
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Slevin, Elise, Leonardo Baiocchi, Nan Wu, Burcin Ekser, Keisaku Sato, Emily Lin, Ludovica Ceci, et al. "Kupffer Cells." American Journal of Pathology 190, no. 11 (November 2020): 2185–93. http://dx.doi.org/10.1016/j.ajpath.2020.08.014.

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10

Ikejima, Kenichi, Nobuyuki Enomoto, Vitor Seabra, Ayako Ikejima, David A. Brenner, and Ronald G. Thurman. "Pronase destroys the lipopolysaccharide receptor CD14 on Kupffer cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 3 (March 1, 1999): G591—G598. http://dx.doi.org/10.1152/ajpgi.1999.276.3.g591.

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CD14 is a lipopolysaccharide (LPS) receptor distributed largely in macrophages, monocytes, and neutrophils; however, the role of CD14 in activation of Kupffer cells by LPS remains controversial. The purpose of this study was to determine if different methods used to isolate Kupffer cells affect CD14. Kupffer cells were isolated by collagenase (0.025%) or collagenase-Pronase (0.02%) perfusion and differential centrifugation using Percoll gradients and cultured for 24 h before experiments. CD14 mRNA was detected by RT-PCR from Kupffer cell total RNA as well as from peritoneal macrophages. Western blotting showed that Kupffer cells prepared with collagenase possess CD14; however, it was absent in cells obtained by collagenase-Pronase perfusion. Intracellular calcium in Kupffer cells prepared with collagenase was increased transiently to levels around 300 nM by addition of LPS with 5% rat serum, which contains LPS binding protein. This increase in intracellular calcium was totally serum dependent. Moreover, LPS-induced increases in intracellular calcium in Kupffer cells were blunted significantly (40% of controls) when cells were treated with phosphatidylinositol-specific phospholipase C, which cleaves CD14 from the plasma membrane. However, intracellular calcium did not increase when LPS was added to cells prepared by collagenase-Pronase perfusion even in the presence of serum. These cells were viable, however, because ATP increased intracellular calcium to the same levels as cells prepared with collagenase perfusion. Tumor necrosis factor-α (TNF-α) mRNA was increased in Kupffer cells prepared with collagenase perfusion 1 h after addition of LPS, an effect potentiated over twofold by serum; however, serum did not increase TNF-α mRNA in cells isolated via collagenase-Pronase perfusion. Moreover, treatment with Pronase rapidly decreased CD14 on mouse macrophages (RAW 264.7 cells) and Kupffer cells. These findings indicate that Pronase cleaves CD14 from Kupffer cells, whereas collagenase perfusion does not, providing an explanation for why Kupffer cells do not exhibit a CD14-mediated pathway when prepared with procedures using Pronase. It is concluded that Kupffer cells indeed contain a functional CD14 LPS receptor when prepared gently.
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Dissertations / Theses on the topic "Kupffer"

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Finckh, Matthias. "Zum Mechanismus der Kupfer-assoziierten Leberschädigung bei der Long-Evans-Cinnamon-Ratte." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964589044.

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Hespeling, Ursula, Kurt Jungermann, and Gerhard P. Püschel. "Feedback-inhibition of glucagon-stimulated glycogenolysis in hepatocyte/kupffer cell cocultures by glucagon-elicited prostaglandin production in kupffer cells." Universität Potsdam, 1995. http://opus.kobv.de/ubp/volltexte/2008/1669/.

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Prostaglandins, released from Kupffer cells, have been shown to mediate the increase in hepatic glycogenolysis by various stimuli such as zymosan, endotoxin, immune complexes, and anaphylotoxin C3a involving prostaglandin (PG) receptors coupled to phospholipase C via a G(0) protein. PGs also decreased glucagon-stimulated glycogenolysis in hepatocytes by a different signal chain involving PGE(2) receptors coupled to adenylate cyclase via a G(i) protein (EP(3) receptors). The source of the prostaglandins for this latter glucagon-antagonistic action is so far unknown. This study provides evidence that Kupffer cells may be one source: in Kupffer cells, maintained in primary culture for 72 hours, glucagon (0.1 to 10 nmol/ L) increased PGE(2), PGF(2 alpha), and PGD(2) synthesis rapidly and transiently. Maximal prostaglandin concentrations were reached after 5 minutes. Glucagon (1 nmol/L) elevated the cyclic adenosine monophosphate (cAMP) and inositol triphosphate (InsP(3)) levels in Kupffer cells about fivefold and twofold, respectively. The increase in glyco gen phosphorylase activity elicited by 1 nmol/L glucagon was about twice as large in monocultures of hepatocytes than in cocultures of hepatocytes and Kupffer cells with the same hepatocyte density. Treatment of cocultures with 500 mu mol/L acetylsalicylic acid (ASA) to irreversibly inhibit cyclooxygenase (PGH-synthase) 30 minutes before addition of glucagon abolished this difference. These data support the hypothesis that PGs produced by Kupffer cells in response to glucagon might participate in a feedback loop inhibiting glucagon-stimulated glycogenolysis in hepatocytes.
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Adé, Kémy. "Kupffer Cell Maintenance in Tissue Repair and Ageing." Electronic Thesis or Diss., Sorbonne université, 2021. http://www.theses.fr/2021SORUS312.

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Les cellules de Kupffer (KCs) sont les macrophages résidents du foie. Phagocytes professionnels, ils sont au cœur du système immunitaire inné, première ligne de défense de l’organisme contre les agressions. Ils participent également au maintien de l’homéostasie tissulaire. Des travaux récents ont permis de comprendre leur origine. On sait maintenant que, à l’instar de la majorité des macrophages résidant dans les tissus, les KCs émergent durant la vie embryonnaire à partir des précurseurs érythro-myeloïdes (EMP), colonisent le foie durant le développement et y persistent à l’âge adulte. Cependant, en cas d’inflammation, ils sont rejoints par des macrophages différenciés à partir des monocytes circulants descendants des cellules souches hématopoïétiques. J’ai étudié la capacité des KCs à persister tout au long de la vie, y compris chez des souris gériatriques. En utilisant la cytométrie en flux et des techniques de traçage de lignées, j’ai montré que la densité des KCs diminuait avec l’âge sans compensation par les monocytes circulants. Un séquençage ARN, l’analyse de mutants TicamLPS2 et des expériences d’inflammation répétées induites par un analogue viral ont mis en lumière le possible rôle de l’inflammation dans ce phénotype. Ce dernier corrélait avec des altérations fonctionnelles. L’étude de la persistance des KCs dans un modèle de lésion aiguë du foie induite par le paracétamol et après déplétion des KCs par un antagoniste du récepteur CSF1R a montré que les KCs étaient capables de persister ou se reconstituer sans contribution de la circulation. Ces expériences établissent des outils pour une caractérisation des fonctions des KCs en contexte pathologique
Kupffer cells (KCs) are resident macrophages of the liver. Professional phagocytes of the innate immune system, they take part in the first line of defence against infections and injury. They also actively regulate liver homeostasis. Recent works have elucidated their origin. We now know that, like most other tissue resident macrophages, KCs develop during embryonic life from Erythro-Myeloid Progenitors (EMPs), seed the liver during development and persist there in adulthood. During inflammation, however, they can be joined by recently differentiated macrophages that arise from circulating monocytes belonging to the Haematopoietic Stem Cell (HSC) descendance. Here I studied the ability of mouse KCs to maintain themselves throughout life, and into old age. Using flow cytometry and fate mapping strategies, we showed that KC density decreased over time and was not compensated by recruitment of circulating cells. RNA sequencing, analysis of TicamLPS2 mutants and Poly (I:C)-induced repeated inflammation experiments highlighted the contribution of inflammation to the ageing phenotype. This phenotype correlated with lipid and senescent cell accumulation. We further studied KC maintenance in acetaminophen induced liver injury and after depletion induced by a CSF1R antagonist. In both contexts, KCs were able to maintain themselves through local proliferation without significant input from circulating cells. These experiments will provide a framework for the better characterisation of KC functions in injury and disease
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Durquet-Perelman, Claire. "Repercussions d'un traitement par les oestrogenes sur les fonctions des cellules de kupffer in vivo et in vitro." Université Louis Pasteur (Strasbourg) (1971-2008), 1989. http://www.theses.fr/1989STR1M074.

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Burlak, Christopher II. "Analysis of Porcine Kupffer Cell Recognition of Human Erythrocytes." University of Toledo Health Science Campus / OhioLINK, 2003. http://rave.ohiolink.edu/etdc/view?acc_num=mco1083268448.

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Leroux, Anne. "Rôle du macrophage dans les étapes précoces de la stéatohépatite non alcoolique (NASH)." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA114829.

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L’obésité est à l’origine de la première cause de maladies hépatiques dans les pays occidentaux. Les lésions hépatiques s’étendent de la stéatose isolée et réversible à la stéatohépatite (NASH), la fibrose, la cirrhose jusqu’au carcinome hépatocellulaire. Aucun traitement pharmacologique n’a montré son efficacité pour éviter cette évolution. La compréhension des mécanismes à l’origine du processus inflammatoire est donc un élément clef pour le développement de nouvelles voies thérapeutiques. Nous avons précédemment montré dans un modèle murin d’obésité que la stéatose induit un recrutement accru de lymphocytes par le foie. Les cellules de Kupffer représentent jusqu’à 20% des cellules immunitaires du foie. Elles peuvent présenter différents phénotypes : pro-inflammatoire ou anti-inflammatoire. Un phénotype pro-inflammatoire engendre la sécrétion de cytokines/chimiokines pro-inflammatoires favorisant une réponse immune de type Th1 et un recrutement de cellules immunitaires. Les cellules de Kupffer pourraient ainsi être des acteurs majeurs dans les étapes précoces du développement de la maladie.Le but de ce travail a été d’étudier le phénotype des cellules de Kupffer au stade de la stéatose et le rôle des lipides dans ce phénotype.Nous avons montré que l'accumulation de lipides dans les cellules de Kupffer est due à un dérèglement du métabolisme des lipides et de leur trafic. Les cellules de Kupffer chargées de lipides ont un phénotype pro-inflammatoire qui induit le recrutement des lymphocytes durant les premiers stades du développement de la NASH et qui est réversible par l'inhibition de la lipogenèse
We have shown lipid accumulation in fat-laden Kupffer cells is due to a dysregulation of lipid metabolism and trafficking. Fat-laden Kupffer cells are "primed" to recruit lymphocytes and exhibit a pro-inflammatory phenotype at the stage of steatosis, which is reversible with inhibition of lipogenesis
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Nashat, Khalid Hashim. "Kinetic studies of the hepatic reticuloendothelial system." Thesis, University of Sheffield, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.280637.

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Raddi, Najat. "Rôle de la fibre adénovirale dans le tropisme hépatique et la toxicité des vecteurs adénoviraux." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T029.

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Les adénovirus (Ad) sont parmi les vecteurs les plus utilisés en thérapie génique. Cependant, les données d’essais pré-Cliniques et cliniques ont montré qu’ils induisaient une forte toxicité hépatique consécutive à leur tropisme hépatique, une réponse inflammatoire et une forte thrombocytopénie. Différents travaux avaient montré que l’interaction de l’Ad avec le facteur de la coagulation X (FX).était responsable de la transduction in vivo des hépatocytes après administration systémique des vecteurs Ad. Cependant, des résultats précédents du laboratoire avaient montré également que le pseudotypage d’une autre protéine de capside, la fibre, permettait de réduire la transduction hépatique. Dans le but de mieux comprendre le rôle de la fibre dans le tropisme et la toxicité des Ad, nous avons comparé des Ad recombinants pseudotypés pour tout (tige et tête de la fibre : AdF3) ou partie (tige : AdS3K5) de la fibre Ad3 avec un Ad5 à capside non modifiée (Adwt). Après administration systémique chez la souris, l’AdF3 et l’AdS3K5 induisent une plus faible expression du transgène dans le foie et la rate comparativement à l’Ad5wt. Cette réduction ne résulte ni d’un défaut de capture de ces vecteurs dans le foie ni de leur incapacité à utiliser le FX. Cependant, nos résultats ont révélé que les Ad pseudotypés par la fibre Ad3 étaient capturés de façon plus importante par les cellules de Kupffer. Nous avons montré que cette capture était une propriété intrinsèque de la fibre Ad3 puisqu’elle était observée également après administration systémique d’un Ad de sérotype 3. De façon intéressante, les Ad pseudotypés par la fibre Ad3 restent capables de transférer des gènes dans les tumeurs aussi efficacement que l’Adwt.Dans la deuxième partie de nos travaux, nous avons cherché à mieux comprendre les mécanismes de la thrombocytopénie consécutive à l’administration d’Ad. Nous avons défini la cinétique de la thrombocytopénie ainsi que l’effet de la dose virale. Nous avons montré que certains facteurs de l’hôte comme les facteurs de la coagulation ou la rate n’étaient pas impliqués dans la thrombocytopénie. De façon intéressante, nous avons montré que la fibre Ad5 jouait un rôle dans l’induction de la baisse plaquettaire puisque l’administration des virus à fibre Ad3 n’induisait plus de forte baisse plaquettaire. Parallèlement, nous avons observé un profil inflammatoire associé à l’administration des Ad à fibre modifiée beaucoup plus réduit que celui de l’Adwt. Nos travaux en cours évaluent l’existence possible d’une corrélation entre la production de cytokines/chimiokines et la thrombocytopénie.L’ensemble de ces résultats montre que le pseudotypage des Ad5 par la fibre de l’Ad3 permet de réduire leur toxicité et de limiter la réponse inflammatoire tout en conservant un transfert de gènes efficace dans les tumeurs. L’introduction de ce type de modification de capside dans les Ad oncolytiques devrait permettre de conserver leur capacité à se répliquer dans les tumeurs tout en limitant les toxicités liées à leur dissémination par voie systémique
To date adenoviruses (Ad) are the most used vectors in gene therapy. However, Ad use is hampered by a strong liver tropism that leads to hepatotoxicity, a strong inflammatory response and the induction of thrombocytopenia. Binding of Ad hexon to coagulation factor X (FX) is responsible for hepatocyte transduction in vivo. As a consequence, mutation of hexon protein abrogates Ad interaction with FX and reduces liver transduction. However, previous results of our lab have demonstrated that Ad5 pseudotyping with fiber Ad3 also resulted in significant reduction of liver transduction. To understand how fiber modification affects in vivo Ad tropism, we used two pseudotyped viruses with whole (AdF3) or only the shaft (AdS3K5) of Ad3 fiber.Following systemic delivery of fiber-Modified Ads, a reduced transduction was observed 2 days p.i. in liver and spleen. This reduction was not due to the impairment of fiber-Modified Ads liver entry or FX use in vivo. Remarkably, after Kupffer cells depletion, a restored transgene expression level was observed, suggesting that fiber-Modified Ads are strongly uptaken by Kupffer cells. We have demonstrated that this strong uptake is an Ad3 intrinsic property since Ad3 was also strongly uptaken by Kupffer cells. Interestingly, fiber-Modified Ads transduce tumours as efficiently as Ad5. In the second part of this work, we aimed to better understand the mechanism of Ad-Induced thrombocytopenia. We first defined the kinetic and dose-Dependence of Ad-Induced thrombocytopenia. Then, we have shown that factors of the host such as the coagulation factors and the spleen were not involved in the thrombocytopenia development. Interestingly, we demonstrated o role for Ad5 in this platelet count reduction since fiber-Modified Ad induced only a modest thrombocytopenia. In parallel, we have observed a reduced production of inflammatory cytokine and chemokine following fiber-Modified Ad administration. Experiments are ongoing to investigate a possible correlation between inflammatory responses and thrombocytopenia. Altogether, our findings demonstrate that Ad5 pseudotyping with Ad3 fiber allows à reduced toxicity and inflammatory response while tumour transduction efficacy is remained. Therfore, oncolytic Ad pseudotyped with Ad3 fiber might be potent tool in tumor virotherapy while limiting risk of toxicity
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9

Kennedy, James Andrew. "Characterization and modulation of Kupffer cell function in experimental obstructive jaundice." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387894.

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Crunkhorn, Sarah Elizabeth. "Role of Kupffer cells in xenobiotic induced liver growth in rats." Thesis, University of Surrey, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250964.

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Books on the topic "Kupffer"

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Aouadi, Myriam, and Valerio Azzimato, eds. Kupffer Cells. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0704-6.

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R, Billiar Timothy, and Curran Ronald D, eds. Hepatocyte and Kupffer Cell interactions. Boca Raton: CRC Press, 1992.

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International, Kupffer Cell Symposium (3rd 1985 Strasbourg France). Cells ofthe hepatic sinusoid. Rijwsojk, The Netherlands: Kupffer Cell Foundation, 1986.

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Badger, Ian Laurence Russell. A study of Kupffer cell function in liver transplantation. Birmingham: University of Birmingham, 1992.

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Charles, Balabaud, and Bioulac-Sage Paulette, eds. Sinusoids in human liver: Health and disease : editors, Paulette Bioulac-Sage, Charles Balabaud. Rijswijk, The Netherlands: Kupffer Cell Foundation, 1988.

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Regulation of vitamin A homeostasis by the stellate cell (vitamin A-storing cell) system. New York: Nova Biomedical Books, 2011.

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Lummer, Rupert. Harry Kupfer. Frankfurt am Main: Fischer Taschenbuch Verlag, 1989.

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1958-, Lewin Michael, ed. Harry Kupfer. Wien: Europaverlag, 1988.

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In Kupfer gestochen: Observationen. Frankfurt am Main: Suhrkamp, 1987.

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Kneubühler, Peter. Kupfer Druck: Peter Kneubühler, Kupferdruck, Zürich. Baden: L. Müller, 1990.

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Book chapters on the topic "Kupffer"

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Kiyani, Amirali, and Ekihiro Seki. "Kupffer cells." In Signaling Pathways in Liver Diseases, 61–72. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118663387.ch4.

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Thomas, Peter. "Kupffer Cells." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_3251-2.

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Kmieć, Zbigniew. "Kupffer Cells." In Cooperation of Liver Cells in Health and Disease, 21–28. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56553-3_4.

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Thomas, Peter. "Kupffer Cells." In Encyclopedia of Cancer, 2429–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_3251.

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Thomas, Peter. "Kupffer Cells." In Encyclopedia of Cancer, 1963–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3251.

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Gooch, Jan W. "Kupffer Cells." In Encyclopedic Dictionary of Polymers, 903. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14081.

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Gandhi, Chandrashekhar R. "Kupffer Cells." In Molecular Pathology Library, 81–95. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7107-4_6.

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Oosterhuis, Harry. "Kupffer, Elisár von." In Who's Who in Gay and Lesbian History, 248–49. 2nd ed. London: Routledge, 2020. http://dx.doi.org/10.4324/9781003070900-261.

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Barreby, Emelie, and Connie Xu. "Kupffer Cell mRNA Sequencing." In Methods in Molecular Biology, 27–44. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0704-6_5.

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Crispe, Ian Nicholas. "Kupffer Cells in Immune Tolerance." In Encyclopedia of Medical Immunology, 623–28. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_193.

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Conference papers on the topic "Kupffer"

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Owumi, Solomon E. "Abstract A45: Kupffer cell and EtOH DNA synthesis." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Dec 6–9, 2009; Houston, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-09-a45.

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Van Hamme, Evelien. "The liver revisited: CLEM reveals the Kupffer cell niche." In European Microscopy Congress 2020. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.emc2020.602.

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Zhang, J., A. Wieser, H. Li, J. Mayerle, AL Gerbes, and CJ Steib. "Pretreatment with Zinc protects Kupffer cells following administration of microbial products." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695375.

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GUARDIGLI, M., A. RODA, R. ALDINI, A. MARANGONI, and R. CEVENINI. "EVALUATION OF REACTIVE OXYGEN SPECIES PRODUCTION IN KUPFFER CELLS BY CHEMILUMINESCENCE." In Bioluminescence and Chemiluminescence - Progress and Current Applications - 12th International Symposium on Bioluminescence (BL) and Chemiluminescence (CL). WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812776624_0055.

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Peiseler, Moritz, Catharina Demske, Wiebke Werner, Linda Hammerich, Frank Tacke, and Felix Heymann. "Tim4high expression identifies a Kupffer cell subset with enhanced catching proficiency." In 38. Jahrestagung der Deutsche Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0041-1740805.

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Dewidar, B., S. Hammad, HL Weng, MP Ebert, JG Hengstler, and S. Dooley. "Jagged-1 expression in stressed hepatocytes enhances phagocytic activity of Kupffer cells." In Viszeralmedizin 2017. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1605073.

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Meyer, David, Sara Shum, Mechthild Jonas, Martha Anderson, Joshua Hunter, Nagendra Chemuturi, Nicole Okeley, and Robert Lyon. "Abstract 351: Uptake of antibody-drug conjugates by cultured Kupffer cells can predict pharmacokinetics." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-351.

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Stiles, Bangyan L., Taojian Tu, Lina He, and Mario Alba. "Abstract P048: Steatosis promote liver cancer development by inducing chemokine production from Kupffer cells." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 5-6, 2021. American Association for Cancer Research, 2022. http://dx.doi.org/10.1158/2326-6074.tumimm21-p048.

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Fang, X., and GM Deng. "213 Hepatic deposited igg mediated liver damage through kupffer/natural killer cells and their products." In LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.213.

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Mi, Yu, Feifei Yang, and Andrew Z. Wang. "Abstract 3899: Nanoparticle reduces hepatotoxicity of cancer treatment by controlled release and Kupffer cell uptake." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3899.

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Reports on the topic "Kupffer"

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Kupfer, Monica E. Perceptive Strokes: Women Artists of Panama. Inter-American Development Bank, March 2013. http://dx.doi.org/10.18235/0006215.

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The IDB Cultural Center is proud to host this exhibit honoring the Republic of Panama, host country of the IDB Annual Meeting, which will take place from March 14¿20, 2013. The exhibition highlights the history of modern and contemporary art by Panamanian women and will include paintings, photographs, sculptures, and video art from the 1920s to the present. The 22 artworks, selected by Panamanian curator Dr. Monica E. Kupfer, reveal the ways in which a varied group of female artists have experienced and represented significant geopolitical events in the nation¿s history. Their interpretations also show the position of women in Panamanian society, and their views of themselves through their own and others¿ eyes. Among the artists are: Susana Arias, Beatrix (Trixie) Briceño, Fabiola Buritica, Coqui Calderón, María Raquel Cochez, Donna Conlon, Isabel De Obaldía, Sandra Eleta, Ana Elena Garuz, Teresa Icaza, Iraida Icaza, Amelia Lyons de Alfaro, Lezlie Milson, Rachelle Mozman, Roser Muntañola de Oduber, Amalia Rossi de Jeanine, Olga Sánchez, Olga Sinclair, Victoria Suescum, Amalia Tapia, Alicia Viteri, and Emily Zhukov.
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A Century of Painting in Panama. Inter-American Development Bank, November 2003. http://dx.doi.org/10.18235/0005898.

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An exhibition of exceptional paintings by 25 outstanding artists selected from a survey of a wide-ranging group of art connoisseurs, historians, critics, professors and art dealers in Panama gave the public an overview of the development of painting in Panama over the 20th century. The selection included early 20th century artists such as Roberto Lewis, Humberto Ivaldi, and Manuel Amador; and painters from Mid-century and end of the 20th century. Dr. Mónica E. Kupfer, Former Curator of the Panama's Museum of Contemporary Art, was invited as Associate Curator for this exhibition.
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