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1.

001-es BibID:BIBFORM028423
Első szerző:Ajuebor, Maureen N.
Cím:Role of resident peritoneal macrophages and mast cells in chemokine production and neutrophil migration in acute inflammation : evidence for an inhibitory loop involving endogenous IL-10 / Maureen N. Ajuebor, Anuk M. Das, László Virág, Roderick J. Flower, Csaba Szabó, Mauro Perretti
Dátum:1999
ISSN:1550-6606
Megjegyzések:The roles played by resident macrophages (Mphi) and mast cells (MCs) in polymorphonuclear leukocyte (PMN) accumulation and chemokine production within the mouse peritoneal cavity in response to administration of zymosan (0.2 and 1 mg), LPS (1 mg/kg), and thioglycolate (0.5 ml of a 3% suspension) were investigated. A marked reduction (>95%) in intact MC numbers was obtained by pretreatment with the MC activator compound 48/80, whereas resident Mphi were greatly diminished (>85%) by a 3-day treatment with liposomes encapsulating the cytotoxic drug dichloromethylene-bisphosphonate. No modulation of thioglycolate-induced inflammation was seen with either pretreatment. Removal of either MCs or Mphi attenuated LPS-induced PMN extravasation without affecting the levels of the chemokines murine monocyte chemoattractant protein-1 and KC measured in the lavage fluids. In contrast, MC depletion inhibited PMN accumulation and murine monocyte chemoattractant protein-1 and KC production in the zymosan peritonitis model. Removal of Mphi augmented the accumulation of PMN elicited by the latter stimulus. This was due to an inhibitory action of Mphi-derived IL-10 because there was 1) a time-dependent release of IL-10 in the zymosan exudates; 2) a reduction in IL-10 levels following Mphi, but not MC, depletion; and 3) an increased PMN influx and chemokine production in IL-10 knockout mice. In conclusion, we propose a stimulus-dependent role of resident MCs in chemokine production and the existence of a regulatory loop between endogenous IL-10 and the chemokine-mediated cellular component of acute inflammation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Immunology 162 : 3 (1999), p. 1685-1691. -
További szerzők:Das, Anuk M. Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Flower, Roderick J. Szabó Csaba (1967-) (orvos) Perretti, Mauro
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2.

001-es BibID:BIBFORM028397
Első szerző:Eaves-Pyles, Tonyia
Cím:Flagellin, a novel mediator of Salmonella-induced epithelial activation and systemic inflammation : I kappa B alpha degradation, induction of nitric oxide synthase, induction of proinflammatory mediators, and cardiovascular dysfunction / Tonyia Eaves-Pyles, Kanneganti Murthy, Lucas Liaudet, László Virág, Gary Ross, Francisco Garcia Soriano, Csaba Szabó, Andrew L. Salzman
Dátum:2001
ISSN:1550-6606
Megjegyzések:Gram-negative sepsis is mediated by the actions of proinflammatory genes induced in response to microbes and their products. We report that flagellin, the monomeric subunit of flagella, is a potent proinflammatory species released by Salmonella. Flagellin (1 microgram/ml) induces IkappaBalpha degradation, NF-kappaB nuclear translocation, and inducible NO synthase expression in cultured intestinal epithelial cells (IEC). Aflagellic Salmonella mutants do not induce NF-kappaB activation or NO production by cultured IEC. Antiserum to flagellin blocks NO production in IEC induced by medium conditioned by a variety of motile Gram-negative enteric pathogens (Escherichia coli, Salmonella muenchen, Serratia marcescens, Proteus mirabilis, and Proteus vulgaris). Flagellin, when injected systemically (approximately 10 microgram/mouse), induces systemic inflammation characterized by the systemic expression of a range of proinflammatory cytokines and chemokines and of inducible NO synthase. At higher doses (approximately 300 microgram/mouse), flagellin induces shock, characterized by hypotension, reduced vascular contractility in mice, and death. The effects of flagellin do not diminish in C3H/HeJ LPS-resistant mice, indicating that the Toll-like receptor-4 receptor is not involved in flagellin's actions. In LPS-resistant mice, i.p. injection of S. dublin flagellin or medium conditioned by wild-type S. dublin induces serum IFN-gamma and TNF-alpha, whereas medium conditioned by aflagellic mutants has no effect. Flagellin can be detected in the blood of rats with septic shock induced by live bacteria at approximately 1 microg/ml. We propose that flagellin released by Gram-negative pathogens may contribute to the inflammatory response by an LPS- and Toll-like receptor-4-independent pathway.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Immunology 166 : 2 (2001), p. 1248-1260. -
További szerzők:Murthy, Kanneganti G. Liaudet, Lucas Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Ross, Gary Soriano, Francisco Garcia Szabó Csaba (1967-) (orvos) Salzman, Andrew L.
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3.

001-es BibID:BIBFORM028537
Első szerző:Haskó György (biokémikus)
Cím:The crucial role of IL-10 in the suppression of the immunological response in mice exposed to staphylococcal enterotoxin B / György Haskó, László Virág, Gregory Egnaczyk, Andrew L. Salzman, Csaba Szabó
Dátum:1998
ISSN:0014-2980
Megjegyzések:Staphylococcal enterotoxin B (SEB), a bacterial superantigen, activates the immune system resulting in a burst of pro- and anti-inflammatory cytokines. A central anti-inflammatory mediator in this process is IL-10. Using IL-10-deficient C57BL/6 (IL-10 KO) mice, we studied the role of endogenous IL-10 in the regulation of the immune response to SEB. SEB (100 microg) induced the release of IL-10 in control C57BL/6 [IL-10 wild type (WT)] mice, but not in their IL-10 KO counterparts. SEB-evoked plasma levels of TNF-alpha, IL-1beta, IL-2, IL-6, IL-12 and IFN-gamma were significantly higher in the IL-10 KO mice than in the WT animals. The release of macrophage inflammatory proteins-1alpha and -2 was also enhanced in the IL-10 KO mice. Further, upon SEB challenge, mice deficient in IL-10 produced higher levels of nitric oxide than the WT animals. IL-10 deficiency resulted in a marked enhancement of the SEB-induced apoptosis of thymocytes. Finally, IL-10 KO mice were more susceptible to SEB-induced lethal shock than their WT controls. These results show that IL-10 plays an important immunoregulatory role in the response to a superantigenic stimulus, by dampening of the shock-inducing inflammatory response and early activation-induced cell death elicited by SEB.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
IL-10
cytokine
inflammation
IL-12
macrophage inflammatory protein
külföldön készült közlemény
Megjelenés:European Journal of Immunology 28 : 4 (1998), p. 1417-1425. -
További szerzők:Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Egnaczyk, Greg Salzman, Andrew L. Szabó Csaba (1967-) (orvos)
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4.

001-es BibID:BIBFORM028555
Első szerző:Haskó György (biokémikus)
Cím:Ecto-5'-nucleotidase (CD73) decreases mortality and organ injury in sepsis / György Haskó, Balázs Csóka, Balázs Koscsó, Rachna Chandra, Pál Pacher, Linda F. Thompson, Edwin A. Deitch, Zoltán Spolarics, László Virág, Pál Gergely, Rolando H. Rolandelli, Zoltán H. Németh
Dátum:2011
ISSN:0022-1767
Megjegyzések:The extracellular concentrations of adenosine are increased during sepsis, and adenosine receptors regulate the host's response to sepsis. In this study, we investigated the role of the adenosine-generating ectoenzyme, ecto-5'-nucleotidase (CD73), in regulating immune and organ function during sepsis. Polymicrobial sepsis was induced by subjecting CD73 knockout (KO) and wild type (WT) mice to cecal ligation and puncture. CD73 KO mice showed increased mortality in comparison with WT mice, which was associated with increased bacterial counts and elevated inflammatory cytokine and chemokine concentrations in the blood and peritoneum. CD73 deficiency promoted lung injury, as indicated by increased myeloperoxidase activity and neutrophil infiltration, and elevated pulmonary cytokine levels. CD73 KO mice had increased apoptosis in the thymus, as evidenced by increased cleavage of caspase-3 and poly(ADP-ribose) polymerase and increased activation of NF-B. Septic CD73 KO mice had higher blood urea nitrogen levels and increased cytokine levels in the kidney, indicating increased renal dysfunction. The increased kidney injury of CD73 KO mice was associated with augmented activation of p38 MAPK and decreased phosphorylation of Akt. Pharmacological inactivation of CD73 in WT mice using α, β-methylene ADP augmented cytokine levels in the blood and peritoneal lavage fluid. These findings suggest that CD73-derived adenosine may be beneficial in sepsis.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal Of Immunology 187 : 8 (2011), p. 4256-4267. -
További szerzők:Csóka Balázs (1975-) (biokémikus) Koscsó Balázs Chandra, Rachna Pacher Pál Thompson, Linda F. Deitch, Edwin A. Spolarics Zoltán Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Gergely Pál (1947-) (biokémikus) Rolandelli, Rolando H. Németh Zoltán H.
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DOI
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5.

001-es BibID:BIBFORM028413
Első szerző:Haskó György (biokémikus)
Cím:Inosine inhibits inflammatory cytokine production by a posttranscriptional mechanism and protects against endotoxin-induced shock / György Haskó, David G. Kuhel, Zoltán H. Németh, Jon G. Mabley, Robert F. Stachlewitz, László Virág, Zsolt Lohinai, Garry J. Southan, Andrew L. Salzman, Csaba Szabo
Dátum:2000
ISSN:1550-6606
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Journal of Immunology 164 : 2 (2000), p. 1013-1019. -
További szerzők:Kuhel, David G. Németh Zoltán H. Mabley, Jon G. Stachlewitz, Robert Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Lohinai Zsolt Southan, Garry J. Salzman, Andrew L. Szabó Csaba (1967-) (orvos)
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6.

001-es BibID:BIBFORM028557
Első szerző:Koscsó Balázs
Cím:Adenosine Augments IL-10 Production by Microglial Cells through an A2B Adenosine Receptor-Mediated Process / Balázs Koscsó, Balázs Csóka, Zsolt Selmeczy, Leonóra Himer, Pál Pacher, László Virág, György Haskó
Dátum:2012
ISSN:0022-1767
Megjegyzések:Microglia are activated by pathogen-associated molecular patterns and produce proinflammatory cytokines, such as TNF-alfa, IL-6, and IL-12, and the anti-inflammatory cytokine IL-10. Adenosine is an endogenous purine nucleoside and a ligand of four G protein-coupled adenosine receptors (ARs), which are the A(1)AR, A(2A)AR, A(2B)AR, and A(3)AR. ARs have been shown to suppress TNF-alfa production by microglia, but their role in regulating IL-10 production has not been studied. In this study, we demonstrate that adenosine augments IL-10 production by activated murine microglia while suppressing the production of proinflammatory cytokines. Because the order of potency of selective AR agonists in inducing IL-10 production was NECA > IB-MECA > CCPA > CGS21680, and the A(2B)AR antagonist MRS1754 prevented the effect of NECA, we conclude that the stimulatory effect of adenosine on IL-10 production is mediated by the A(2B)AR. Mechanistically, adenosine augmented IL-10 mRNA accumulation by a transcriptional process. Using mutant IL-10 promoter constructs we showed that a CREB-binding region in the promoter mediated the augmenting effect of adenosine on IL-10 transcription. Chromatin immunoprecipitation analysis demonstrated that adenosine induced CREB phosphorylation at the IL-10 promoter. Silencing CREB using lentivirally delivered short hairpin RNA blocked the enhancing effect of adenosine on IL-10 production, confirming a role for CREB in mediating the stimulatory effect of adenosine on IL-10 production. In addition, adenosine augmented IL-10 production by stimulating p38 MAPK. Collectively, our results establish that A(2B)ARs augment IL-10 production by activated murine microglia.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal of Immunology 188 : 1 (2012), p. 445-453. -
További szerzők:Csóka Balázs (1975-) (biokémikus) Selmeczy Zsolt Himer Leonóra Pacher Pál Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Haskó György (1967-) (biokémikus)
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7.

001-es BibID:BIBFORM028439
Első szerző:Virág László (biokémikus, sejtbiológus, farmakológus)
Cím:Poly(ADP-ribose) synthetase activation mediates mitochondrial injury during oxidant-induced cell death / László Virág, Andrew L. Salzman, Csaba Szabó
Dátum:1998
ISSN:1550-6606
Megjegyzések:Reactive oxidant species are important mediators of tissue injury in shock, inflammation, and reperfusion injury. The actions of a number of these oxidants (e.g., hydroxyl radical and peroxynitrite, a reactive oxidant produced by the reaction of nitric oxide and superoxide) are mediated in part by the activation of the nuclear nick sensor enzyme, poly(ADP)-ribose synthetase (PARS), with consequent cellular energy depletion. Here we investigated whether PARS activation contributes to the mitochondrial alterations in cells exposed to oxidants. Authentic peroxynitrite (20 microM), the peroxynitrite-generating compound 3-morpholinosidnonimine, the combination of pyrogallol and S-nitroso-N-acetyl-D,L-penicillamine, as well as hydrogen peroxide induced a time- and dose-dependent decrease in mitochondrial transmembrane potential (delta psi(m)) in thymocytes, as determined by flow cytometry using the mitochondrial potential sensitive dyes DiOC6(3) and JC-1. A time- and dose-dependent increase in secondary reactive oxygen intermediate production and loss of cardiolipin, an indicator of mitochondrial membrane damage, were also observed, as measured by flow cytometry using the fluorescent dyes dihydroethidine and nonyl-acridine orange, respectively. Inhibition of PARS by 3-aminobenzamide or 5-iodo-6-amino-1,2-benzopyrone attenuated peroxynitrite-induced delta psi(m) reduction, secondary reactive oxygen intermediate generation, cardiolipin degradation, and intracellular calcium mobilization. Furthermore, thymocytes from PARS-deficient animals were protected against the peroxynitrite- and hydrogen peroxide-induced functional and ultrastructural mitochondrial alterations. In conclusion, mitochondrial perturbations during oxidant-mediated cytotoxicity are, to a significant degree, related to PARS activation rather than to direct effects of the oxidants on the mitochondria.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal of Immunology. - 161 : 7 (1998), p. 3753-3759. -
További szerzők:Salzman, Andrew L. Szabó Csaba (1967-) (orvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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