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1.

001-es BibID:BIBFORM028554
Első szerző:Ajuebor, Maureen N.
Cím:Regulation of macrophage inflammatory protein-1 alpha expression and function by endogenous interleukin-10 in a model of acute inflammation / Maureen N. Ajuebor, Anuk M. Das, László Virág, Csaba Szabó, Mauro Perretti
Dátum:1999
ISSN:0006-291X
Megjegyzések:In this study we have determined the role of endogenous interleukin (IL)-10 on leucocyte recruitment and production of the CC chemokine macrophage inflammatory protein-1alpha (MIP-1alpha) in a murine model of acute inflammation. Intraperitoneal injection of zymosan produced a dose-dependent cellular infiltration which was concomitant with MIP-1alpha release in the lavage fluids. Release of this chemokine had a functional role since treatment of mice with a specific anti-MIP-1alpha antibody reduced both neutrophil and monocyte accumulation into the peritoneal cavity. An unexpected increase in cell influx and MIP-1alpha production was measured following depletion of resident peritoneal macrophages, as achieved by a 3-day liposome treatment. A similar result was obtained when the zymosan peritonitis response was elicited in IL-10 knock-out mice. In summary we propose a functional cross talk between endogenous IL-10 and this CC chemokine during the host inflammatory response.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Biochemical And Biophysical Research Communications 255 : 2 (1999), p. 279-282. -
További szerzők:Das, Anuk M. Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Szabó Csaba (1967-) (orvos) Perretti, Mauro
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2.

001-es BibID:BIBFORM028543
Első szerző:Ajuebor, Maureen N.
Cím:Role of inducible nitric oxide synthase in the regulation of neutrophil migration in zymosan-induced inflammation / M. N. Ajuebor, L. Virág, R. J. Flower, M. Perretti, Cs. Szabó
Dátum:1998
ISSN:0019-2805
Megjegyzések:In the present study, by comparing the responses in wild-type mice and mice lacking the inducible (or type 2) nitric oxide synthase (iNOS), we investigated the role played by iNOS in the regulation of polymorphonuclear granulocyte (PMN) accumulation and chemokine production in the mouse peritoneal cavity in response to administration of zymosan (0.2 mg). Zymosan injection induced the production of nitric oxide, and triggered a time-dependent PMN immigration into the peritoneal cavity. This response was associated with increases in the level of the chemokines macrophage inflammatory protein (MIP)-1alpha, MIP-2, monocyte chemo-attractant protein (MCP)-1 and cytokine-induced neutrophil chemo-attractant (KC), as measured in the peritoneal cavities. Injection of zymosan also induced a time-dependent increase in the production of the anti-inflammatory cytokine interleukin-10 (IL-10) in the peritoneal cavity. When comparing the response between wild-type and iNOS knockout (KO) mice, we observed that the low-level PMN accumulation measured at 1 hr was slightly but significantly increased in the absence of functional iNOS. On the other hand, the delayed response (2-4 hr after zymosan) of PMN accumulation was suppressed in the iNOS KO mice. The early enhancement of PMN infiltration in the iNOS-deficient mice was associated with increased peritoneal levels of MIP-2, KC and IL-10 proteins. The delayed suppression of PMN infiltration was associated with reduced MIP-2 and IL-10 levels in the peritoneal cavity. The lack of iNOS did not affect the release of MIP-1alpha and MCP-1 at any of the time-points studied. The current data demonstrate that iNOS regulates the production of certain CXC (but not CC) proinflammatory chemokines, the production of IL-10 and exerts a biphasic regulatory effect on PMN accumulation in zymosan-induced acute inflammation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Immunology 95 : 4 (1998), p. 625-630. -
További szerzők:Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Flower, Roderick J. Perretti, Mauro Szabó Csaba (1967-) (orvos)
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3.

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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4.

001-es BibID:BIBFORM045939
035-os BibID:PMID:12839568
Első szerző:Bakondi Edina (biokémikus, vegyész)
Cím:Role of Intracellular Calcium Mobilization and Cell-Density-Dependent Signaling in Oxidative-Stress-Induced Cytotoxicity in HaCaT Keratinocytes / Edina Bakondi, Mónika Gönczi, Éva Szabó, Péter Bai, Pál Pacher, Pál Gergely, László Kovács, János Hunyadi, Csaba Szabó, László Csernoch, László Virág
Dátum:2003
ISSN:0022-202X
Megjegyzések:Peroxynitrite is a nitric-oxide-derived cytotoxic mediator produced in a broad range of inflammatory conditions, ranging from sunburn erythema to contact hypersensitivity. Our previous work has shown that in HaCaT cells the cytotoxic activity of peroxynitrite involves both apoptotic and necrotic routes with poly(ADP-ribose) polymerase activation serving as a mol-ecular switch diverting the default apoptotic pathway toward necrosis. Nonetheless, keratinocytes are regarded as highly resistant toward environmental noxa including oxidative stress. We set out to investigate the possible role of two parameters, intracellular calcium mobilization and high cell density, in protecting HaCaT cells from peroxynitrite/oxidative-stress-induced cytotoxicity. First we characterized the effect of peroxynitrite on the calcium homeostasis of HaCaT cells and demonstrated that both authentic peroxynitrite and the peroxynitrite generating compound 3-morpholino-sydnonimine triggered an elevation in intracellular calcium levels. Moreover, we established that treatment of cells with the cell-permeable calcium chelator BAPTA-AM provided significant cytoprotection against peroxynitrite- and hydrogen-peroxide-induced cytotoxicity. Furthermore, when cells reached confluence they were highly resistant to the toxic effects of peroxynitrite, hydrogen peroxide, and superoxide. The resistance to oxidative stress provided by calcium chelation and high cell density involved inhibiting the activation of both poly(ADP-ribose) polymerase and caspases. Our data may provide an explanation for the resistance to oxidative stress of superficial, highly differentiated keratinocytes and indicate that basal proliferative keratinocytes are sensitive in vivo targets of oxidative stress injury.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal of Investigative Dermatology. - 121 : 1 (2003), p. 88-95. -
További szerzők:Gönczi Mónika (1974-) (élettanász) Szabó Éva (1965-) (bőrgyógyász, kozmetológus) Bai Péter (1976-) (biokémikus) Pacher Pál Gergely Pál (1947-) (biokémikus) Kovács László (1939-) (élettanász) Hunyadi János (1943-) (bőrgyógyász, kozmetológus, allergológus) Szabó Csaba (1967-) (orvos) Csernoch László (1961-) (élettanász) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus)
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5.

001-es BibID:BIBFORM063940
Első szerző:Brunyánszki Attila (biológus, biotechnológus)
Cím:Mitochondrial poly(ADP-ribose) polymerase : the Wizard of Oz at work / Attila Brunyanszki, Bartosz Szczesny, László Virág, Csaba Szabo
Dátum:2016
ISSN:0891-5849
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Free Radical Biology And Medicine. - 100 (2016), p. 257-270. -
További szerzők:Szczesny, Bartosz Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Szabó Csaba (1967-) (orvos)
Pályázati támogatás:TÁMOP 4.2.4.A/ 2-11/1-2012-0001
TÁMOP
OTKA K112336
OTKA
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6.

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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7.

001-es BibID:BIBFORM028538
Első szerző:Gilad, Eli
Cím:Melatonin inhibits expression of the inducible isoform of nitric oxide synthase in murine macrophages : role of inhibition of NFkappaB activation / Eli Gilad, Hector R. Wong, Basilia Zingarelli, László Virág, Michael O'Connor, Andrew L. Salzman, Csaba Szabó
Dátum:1998
ISSN:0892-6638
Megjegyzések:The role of melatonin as an immunomodulator is well established. Recent reports showed that melatonin exerts protective effects in septic and hemorrhagic shock and in inflammation. The expression of the inducible isoform of nitric oxide synthase (iNOS) makes an important contribution to the pathophysiology of shock and inflammation. We studied, in cultured murine macrophages, the role of melatonin in the regulation of the expression of iNOS and defined the mode of melatonin's action. Our results show that melatonin, at 1 microM-1 mM, decreased the production of nitrite/nitrate (the breakdown products of NO) as well as the production of 6-keto-prostaglandin F1alpha (the major stable breakdown product of prostacyclin) in macrophages stimulated with bacterial lipopolysaccharide (10 microg/ml). We observed that melatonin reduces iNOS steady-state mRNA levels and iNOS protein expression in the same concentration range (1 microM-1 mM). Melatonin, up to 10 mM, exerted only a slight direct inhibitory effect on iNOS activity. Using iNOS promoter-luciferase constructs, we found that melatonin inhibits iNOS promoter activation. Inhibition of iNOS expression was associated with inhibition of activation of the transcription factor nuclear factor kappa B (NFkappaB). We conclude that melatonin inhibits NO production in immunostimulated macrophages mainly by inhibiting the expression of iNOS. This is due to inhibition of iNOS transcription, in part through inhibition of NFkappaB activation. Inhibition of iNOS-derived NO production by melatonin may contribute to the anti-inflammatory effects of this pineal secretory product.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
antioxidants
scavengers
inflammation
gene expression
LPS
mesangial cells
külföldön készült közlemény
Megjelenés:Faseb Journal 12 : 9 (1998), p. 685-693. -
További szerzők:Wong, Hector R. Zingarelli, Basilia Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) O'Connor, Michael Salzman, Andrew L. Szabó Csaba (1967-) (orvos)
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8.

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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9.

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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10.

001-es BibID:BIBFORM028387
Első szerző:Kirov, Mikhail Y.
Cím:Aerosolized linear polyethylenimine-nitric oxide/nucleophile adduct attenuates endotoxin-induced lung injury in sheep / Mikhail Y. Kirov, Oleg V. Evgenov, Vladimir N. Kuklin, László Virág, Pál Pacher, Garry J. Southan, Andrew L. Salzman, Csaba Szabó, Lars J. Bjertnaes
Dátum:2002
ISSN:1073-449X
Megjegyzések:Pulmonary hypertension and edema are mainstays of acute lung injury (ALI). We synthesized linear polyethylenimine-nitric oxide/nucleophile adduct (DS-1), a water-soluble nitric oxide donor, and demonstrated that it is a potent relaxant of precontracted rat aortic rings without inducing desensitization. Moreover, DS-1 does not suppress the viability of human pulmonary epithelial cells in vitro. We also tested whether DS-1 counteracts ALI in endotoxemic sheep. Animals were instrumented for a chronic study. In 16 awake, spontaneously breathing sheep, Escherichia coli endotoxin (10 ng/kg/minute) was infused for 8 hours. From 2 hours of endotoxemia, sheep received either nebulized DS-1 (1 mg/kg/hour) or isotonic saline. DS-1 reduced endotoxin-induced rises in pulmonary arterial and microwedge pressures and vascular resistance index by 40-70%. In parallel, DS-1 decreased the accumulation of extravascular lung water by 60-70% and reduced the increment in right ventricle stroke work index and the falls in right ventricle ejection fraction, stroke volume, and left ventricle stroke work indices. Furthermore, DS-1 reduced venous admixture and improved arterial oxygen saturation. In four healthy animals, DS-1 alone slightly increased arterial oxygenation but had no other effects. Thus, aerosolized DS-1 attenuates endotoxin-induced ALI in sheep by reducing pulmonary hypertension and edema and improving myocardial function and gas exchange.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
acute lung injury
pulmonary circulation
extravascular lung water
nitric oxide donor
endotoxin
külföldön készült közlemény
Megjelenés:American Journal Of Respiratory And Critical Care Medicine 166 : 11 (2002), p. 1436-1442. -
További szerzők:Evgenov, Oleg V. Kuklin, Vladimir N. Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Pacher Pál Southan, Garry J. Salzman, Andrew L. Szabó Csaba (1967-) (orvos) Bjertnaes, Lars J.
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11.

001-es BibID:BIBFORM028371
Első szerző:Komjáti Katalin
Cím:Poly(ADP-ribose) polymerase inhibition protect neurons and the white matter and regulates the translocation of apoptosis-inducing factor in stroke / Katalin Komjáti, John G. Mabley, László Virág, Garry J. Southan, Andrew L. Salzman, Csaba Szabó
Dátum:2004
ISSN:1107-3756
Megjegyzések:Focal cerebral ischemia activates the nuclear protein poly(ADP-ribose) polymerase (PARP). Apoptosis-inducing factor (AIF) is a flavoprotein that is normally confined to the mitochondria, but translocates to the nucleus, as shown by in vitro models of neuronal injury. Using INO-1001, a novel potent inhibitor of PARP, we determined the role of PARP activation in the process of AIF translocation in a rat model of focal cerebral ischemia. The potency of INO-1001 as a PARP inhibitor and its cytoprotective potential in oxidant-challenged human neuronal SK-N-MC cells was first confirmed in vitro. PARP inhibition markedly reduced infarct size and improved neurological status in both transient and permanent models of MCA occlusion in Sprague-Dawley rats, with a therapeutic window of 6 h and 2 h in the transient and permanent ischemia models, respectively. The PARP inhibitor reduced the accumulation of poly(ADP-ribose) in the ischemic/reperfused hemisphere and reduced the accumulation of APP in the white matter of the affected hemisphere, consistently with protection against neuronal necrosis and axonal damage, respectively. Immunohistochemical analysis showed the appearance of AIF labeling in neuronal nuclei of the border zone ischemic area in the striatum after stroke. Cytoplasmatic (axonal) AIF staining was significantly diminished in the necrotic core of the striatum, while it was somewhat enhanced at the borderline ischemic territories of the white matter. Inhibition of PARP with INO-1001 reshifted the location of the apoptotic marker to the axons in the ipsilateral striatum. Thus, PARP inhibition is neuroprotective and regulates the ischemic nuclear translocation of AIF in stroke.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:International Journal Of Molecular Medicine 13 : 3 (2004), p. 373-382. -
További szerzők:Mabley, Jon G. Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Southan, Garry J. Salzman, Andrew L. Szabó Csaba (1967-) (orvos)
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12.

001-es BibID:BIBFORM028548
Első szerző:Liaudet, Lucas
Cím:Inosine exerts a broad range of antiinflammatory effects in a murine model of acute lung injury / Lucas Liaudet, Jon G. Mabley, Pál Pacher, László Virág, Francisco G. Soriano, Anita Marton, György Haskó, Edwin A. Deitch, Csaba Szabó
Dátum:2002
ISSN:0003-4932
Megjegyzések:OBJECTIVE: To investigate the effects of inosine on the acute lung inflammation induced by lipopolysaccharide (LPS) in vivo and on the activation and cytotoxicity elicited by proinflammatory cytokines on human lung epithelial (A549) cells in vitro. SUMMARY BACKGROUND DATA: Inosine is an endogenous purine recently shown to exert immunomodulatory and antiinflammatory effects. METHODS: Mice challenged with intratracheal LPS (50 microg) were treated after 1, 6, and 12 hours with inosine (200 mg/kg intraperitoneal) or vehicle. After 24 hours, bronchoalveolar lavage fluid was obtained to measure proinflammatory (tumor necrosis factor-alpha [TNF-alpha], interleukin [IL]-1beta, IL-6), and antiinflammatory (IL-10, IL-4) cytokines, chemokines (MIP-1alpha and MIP-2), myeloperoxidase activity and total cell counts, nitric oxide production, and proteins. Lung histology and immunohistochemical detection of 3-nitrotyrosine, a marker of nitrosative stress, were performed in inflated-fixed lungs. In vitro, cell viability and production of the chemokine IL-8 were evaluated in A549 cells stimulated with a mixture of cytokines in the presence or absence of inosine. RESULTS: Inosine downregulated the LPS-induced expression of TNF-alpha, IL-1beta, IL-6 and MIP-2 and tended to reduce MIP-1alpha, whereas it enhanced the production of IL-4. Total leukocyte counts, myeloperoxidase, nitric oxide production, and proteins were all significantly decreased by inosine. The purine also improved lung morphology and suppressed 3-nitrotyrosine staining in the lungs after LPS. Inosine attenuated the cytotoxicity and the expression of IL-8 induced by proinflammatory cytokines in A549 cells. CONCLUSIONS: Inosine largely suppressed LPS-induced lung inflammation in vivo and reduced the toxicity of cytokines in lung cells in vitro. These data support the proposal that inosine might represent a useful adjunct in the therapy of acute respiratory distress syndrome.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Annals of Surgery 235 : 4 (2002), p. 568-578. -
További szerzők:Mabley, Jon G. Pacher Pál Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Soriano, Francisco Garcia Marton Anita Haskó György (1967-) (biokémikus) Deitch, Edwin A. Szabó Csaba (1967-) (orvos)
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