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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)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM028376
Első szerző:	Liaudet, Lucas
Cím:	Flagellin from gram-negative bacteria is a potent mediator of acute pulmonary inflammation in sepsis / Lucas Liaudet, Csaba Szabó, Oleg V. Evgenov, Kanneganti G. Murthy, Pál Pacher, László Virág, Jon G. Mabley, Anita Marton, Francisco G. Soriano, Mikhail Y. Kirov, Lars J. Bjertnaes, and Andrew L. Salzman
Dátum:	2003
ISSN:	1073-2322
Megjegyzések:	Flagellin is a recently identified bacterial product that elicits immune response via toll-like receptor 5. Here, we demonstrate that flagellin is an extraordinarily potent proinflammatory stimulus in the lung during sepsis. In vitro, flagellin triggers the production of interleukin (IL)-8 by human lung epithelial (A549) cells, with 50% of the maximal response obtained at a concentration of 2 x 10(-14) M. Flagellin also induces the expression of ICAM-1 in vitro. Intravenous administration of flagellin to mice elicited a severe acute lung inflammation that was significantly more pronounced than following lipopolysaccharide (LPS) administration. Flagellin induced a local release of proinflammatory cytokines, the accumulation of inflammatory cells, and the development of pulmonary hyperpermeability. These effects were associated with the nuclear translocation of the transcription NF-kappaB in the lung. Flagellin remained active in inducing pulmonary inflammation at doses as low as 10 ng/mouse. In the plasma of patients with sepsis, flagellin levels amounted to 7.1 +/- 0.1 ng/mL. Plasma flagellin levels showed a significant positive correlation with the lung injury score, with the alveolar-arterial oxygen difference as well as with the duration of the sepsis. Flagellin emerges as a potent trigger of acute respiratory complications in gram-negative bacterial sepsis.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban endotoxin shock chemokines bacterial infection inflammation lung külföldön készült közlemény
Megjelenés:	Shock 19 : 2 (2003), p. 131-137. -
További szerzők:	Szabó Csaba (1967-) (orvos) Evgenov, Oleg V. Murthy, Kanneganti G. Pacher Pál Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Mabley, Jon G. Marton Anita Soriano, Francisco Garcia Kirov, Mikhail Y. Bjertnaes, Lars J. Salzman, Andrew L.
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM040071
Első szerző:	Soriano, Francisco Garcia
Cím:	Diabetic endothelial dysfunction : the role of poly(ADP-ribose) polymerase activation / Soriano G. F., Virág L., Jagtap P., Szabó E., Mabley J. G., Liaudet L., Marton A., Hoyt D. G., Murthy K. G., Salzman A. L., Southan G. J., Szabó C.
Dátum:	2001
ISSN:	1078-8956
Megjegyzések:	Diabetic patients frequently suffer from retinopathy, nephropathy, neuropathy and accelerated atherosclerosis. The loss of endothelial function precedes these vascular alterations. Here we report that activation of poly(ADP-ribose) polymerase (PARP) is an important factor in the pathogenesis of endothelial dysfunction in diabetes. Destruction of islet cells with streptozotocin in mice induced hyperglycemia, intravascular oxidant production, DNA strand breakage, PARP activation and a selective loss of endothelium-dependent vasodilation. Treatment with a novel potent PARP inhibitor, starting after the time of islet destruction, maintained normal vascular responsiveness, despite the persistence of severe hyperglycemia. Endothelial cells incubated in high glucose exhibited production of reactive nitrogen and oxygen species, consequent single-strand DNA breakage, PARP activation and associated metabolic and functional impairment. Basal and high-glucose-induced nuclear factor-kappaB activation were suppressed in the PARP-deficient cells. Our results indicate that PARP may be a novel drug target for the therapy of diabetic endothelial dysfunction.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Nature Medicine. - 7 : 1 (2001), p. 108-113. -
További szerzők:	Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Jagtap, Prakash Szabó Éva (1965-) (bőrgyógyász, kozmetológus) Mabley, Jon G. Liaudet, Lucas Marton Anita Hoyt, Dale G. Murthy, Kanneganti G. Salzman, Andrew L. Southan, Garry J. Szabó Csaba
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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