Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/22841
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dc.date.accessioned2021-11-29T06:50:15Z-
dc.date.available2021-11-29T06:50:15Z-
dc.date.issued2006-
dc.identifier.citationKıyıcı, M. vd. (2006). ''Lymphocyte subsets and cytokines in ascitic fluid of decompensated cirrhotic patients with and without spontaneous ascites infection''. Journal of Gastroenterology and Hepatology (Australia), 21(6), 963-969.tr_TR
dc.identifier.issn0815-9319-
dc.identifier.urihttps://doi.org/10.1111/j.1440-1746.2006.04229.x-
dc.identifier.urihttps://onlinelibrary.wiley.com/doi/10.1111/j.1440-1746.2006.04229.x-
dc.identifier.urihttp://hdl.handle.net/11452/22841-
dc.description.abstractBackground and Aims: Spontaneous ascites infection is a frequently encountered and important complication of decompensated liver cirrhosis. The immune system plays an important role in the development or eradication of this infection. A number of compositional and functional alterations in immune system cells have been demonstrated in cirrhotic patients; however, there is a lack of knowledge about this issue in ascitic infections. The aim of the present study was to evaluate lymphocyte subsets and levels of some ascitic and lymphocytic intracytoplasmic cytokines in decompensated cirrhotic patients with or without spontaneous ascites infection. Methods: The study population consisted of 45 decompensated cirrhotic patients (32 men, 13 women) with different etiologies. Patients with ascitic polymorphonuclear leukocyte count >= 250/mm(3) and/or positive ascitic bacterial cultures were classified as the 'infected group'. Comparison was made between the infected and non-infected group for the following parameters: ascites leukocyte counts and differentiations; ascitic fluid protein; albumin levels and serum-ascites albumin gradients; flow cytometric detection of cell surface markers for ascitic T, B and natural killer lymphocytes; intracytoplasmic interleukin (IL)-2, IL-4, tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma; levels of ascitic IL-8, IL-10, IL-12 and TNF-alpha; and soluble Fas antigen and soluble Fas ligand. Results: The CD4/CD8 ratio was significantly decreased and expression of T cell receptor-gamma delta was increased in the infected group. Furthermore, ascites TNF-alpha levels were also elevated in this group. Ascitic IL-8, IL-10, IL-12 and TNF-alpha levels were significantly higher in patients with positive ascitic bacterial culture. Conclusions: These results suggest that a cytotoxic, especially Th1, immune response predominates in ascites infections. It also demonstrates that TNF-alpha might be involved in the pathogenesis of ascites infections.tr_TR
dc.language.isoentr_TR
dc.publisherWileytr_TR
dc.rightsinfo:eu-repo/semantics/closedAccesstr_TR
dc.subjectGastroenterology & hepatologytr_TR
dc.subjectCD4tr_TR
dc.subjectLymphocytestr_TR
dc.subjectLigandtr_TR
dc.subjectImmunologytr_TR
dc.subjectReductiontr_TR
dc.subjectCytokinestr_TR
dc.subjectLipopolysaccharidetr_TR
dc.subjectAscites infectionstr_TR
dc.subjectSoluble fastr_TR
dc.subjectHCVtr_TR
dc.subjectSpontaneous bacterial peritonitistr_TR
dc.subjectLiver-diseasetr_TR
dc.titleLymphocyte subsets and cytokines in ascitic fluid of decompensated cirrhotic patients with and without spontaneous ascites infectiontr_TR
dc.typeArticletr_TR
dc.identifier.wos000237740100006tr_TR
dc.identifier.scopus2-s2.0-33744719767tr_TR
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergitr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Gastroenteroloji Anabilim Dalı.tr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/İmmünoloji Anabilim Dalı.tr_TR
dc.contributor.orcid0000-0003-0463-6818tr_TR
dc.contributor.orcid0000-0002-3208-6211tr_TR
dc.identifier.startpage963tr_TR
dc.identifier.endpage969tr_TR
dc.identifier.volume21tr_TR
dc.identifier.issue6tr_TR
dc.relation.journalJournal of Gastroenterology and Hepatologytr_TR
dc.contributor.buuauthorKıyıcı, Murat-
dc.contributor.buuauthorNak, Selim Giray-
dc.contributor.buuauthorBudak, Ferah-
dc.contributor.buuauthorGürel, Selim-
dc.contributor.buuauthorOral, Barbaros-
dc.contributor.buuauthorDolar, Enver-
dc.contributor.buuauthorGülten, Macit-
dc.contributor.researcheridF-4657-2014tr_TR
dc.contributor.researcheridK-7285-2012tr_TR
dc.contributor.researcheridAAI-4213-2021tr_TR
dc.contributor.researcheridAAG-9177-2021tr_TR
dc.identifier.pubmed16724979tr_TR
dc.subject.wosGastroenterology & hepatologytr_TR
dc.indexed.wosSCIEtr_TR
dc.indexed.scopusScopustr_TR
dc.indexed.pubmedPubmedtr_TR
dc.wos.quartileQ3tr_TR
dc.contributor.scopusid6507627491tr_TR
dc.contributor.scopusid6603336505tr_TR
dc.contributor.scopusid6701913697tr_TR
dc.contributor.scopusid7003706434tr_TR
dc.contributor.scopusid7004498001tr_TR
dc.contributor.scopusid6602075084tr_TR
dc.contributor.scopusid6603629209tr_TR
dc.subject.scopusPeritonitis; Rifaximin; Proton Pump Inhibitorstr_TR
dc.subject.emtreeTumor necrosis factor alphatr_TR
dc.subject.emtreeInterleukin 8tr_TR
dc.subject.emtreeInterleukin 4tr_TR
dc.subject.emtreeCytokinetr_TR
dc.subject.emtreeInterleukin 2tr_TR
dc.subject.emtreeInterleukin 12tr_TR
dc.subject.emtreeInterleukin 10tr_TR
dc.subject.emtreeGammatr_TR
dc.subject.emtreeFas antigentr_TR
dc.subject.emtreeFemaletr_TR
dc.subject.emtreeAdulttr_TR
dc.subject.emtreeArticletr_TR
dc.subject.emtreeT lymphocytetr_TR
dc.subject.emtreePriority journaltr_TR
dc.subject.emtreeAscites fluidtr_TR
dc.subject.emtreePriority journaltr_TR
dc.subject.emtreePopulation researchtr_TR
dc.subject.emtreeNeutrophiltr_TR
dc.subject.emtreeMaletr_TR
dc.subject.emtreeLymphocytetr_TR
dc.subject.emtreeLiver cirrhosistr_TR
dc.subject.emtreeHumantr_TR
dc.subject.emtreeFlow cytometrytr_TR
dc.subject.emtreeFemaletr_TR
dc.subject.emtreeControlled studytr_TR
dc.subject.emtreeClinical articletr_TR
dc.subject.emtreeCell differentiationtr_TR
dc.subject.emtreeBacterial counttr_TR
dc.subject.emtreeB lymphocytetr_TR
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