Influence of TH1/TH2 switched immune response on renal ischemia-reperfusion injury

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dc.contributor.authorMarques, Vilmar Paiva [UNIFESP]
dc.contributor.authorGonçalves, Giselle Martins [UNIFESP]
dc.contributor.authorFeitoza, Carla Quarin [UNIFESP]
dc.contributor.authorCenedeze, Marcos Antonio [UNIFESP]
dc.contributor.authorBertocchi, Ana Paula Fernandes [UNIFESP]
dc.contributor.authorDamiao, Marcio Jose [UNIFESP]
dc.contributor.authorPinheiro, Helady Sanders
dc.contributor.authorTeixeira, Vicente Paula Antunes
dc.contributor.authorReis, Marlene Antonia dos
dc.contributor.authorPacheco-Silva, Alvaro [UNIFESP]
dc.contributor.authorCamara, Niels Olsen Saraiva [UNIFESP]
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T12:38:14Z
dc.date.available2016-01-24T12:38:14Z
dc.date.issued2006-01-01
dc.description.abstractBackground/Aims: Recent evidence shows a critical role of the CD4+ T cell with the Th1/Th2 paradigm as a possible effector mechanism in ischemia and reperfusion injury. We hypothesize that a polarized Th1 activation response may negatively influence the renal IRI through its relationship with chemokine production (MCP-1) and with a protective tissue response (HO-1). Methods: We subjected mice to renal ischemia for 45 min using IL-4 and IL-12 knockout C57BL/6. We then measured serum urea levels, performed histomorphometric analysis for tubular necrosis and regeneration, and evaluated the mRNA expression of HO-1, t-bet, Gata-3 and MCP-1 by real-time PCR at 24,48 and 120 h after surgery. Results/Conclusions: the IL-4 knockout mice had a statistically significant rise in serum urea levels post IRI compared with control animals. the IL-12-deficient mice were not affected. the IL-4-deficient mice had a statistically significant increase in tubular injury and impairment in cell regeneration. the IRI in IL-4-deficient mice was accompanied by higher levels of HO-1, t-bet and later up-regulation of MCP-1. These findings suggest that the deleterious effects of the Th1 cell involve increased production of chemokines such as MCP-1. Copyright (c) 2006 S. Karger AG, Basel.en
dc.description.affiliationUniv São Paulo, Inst Biomed Sci, Dept Immunol, BR-05508900 São Paulo, SP, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Div Nephrol, Lab Imunol Clin & Expt, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Div Nephrol, Lab Imunol Clin & Expt, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extentE48-E56
dc.identifierhttp://dx.doi.org/10.1159/000093676
dc.identifier.citationNephron Experimental Nephrology. Basel: Karger, v. 104, n. 1, p. E48-E56, 2006.
dc.identifier.doi10.1159/000093676
dc.identifier.issn1660-2129
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/28613
dc.identifier.wosWOS:000239896100007
dc.language.isoeng
dc.publisherKarger
dc.relation.ispartofNephron Experimental Nephrology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.licensehttp://www.karger.com/Services/RightsPermissions
dc.subjectischemia and reperfusion injuryen
dc.subjectTh1/Th2 cytokinesen
dc.subjectheme oxygenase 1en
dc.titleInfluence of TH1/TH2 switched immune response on renal ischemia-reperfusion injuryen
dc.typeinfo:eu-repo/semantics/article
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