Absence of Fas-L aggravates renal injury in acute Trypanosoma cruzi infection

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dc.contributor.authorOliveira, Gabriel Melo De
dc.contributor.authorMasuda, Masako Oya
dc.contributor.authorRocha, Nazaré N
dc.contributor.authorSchor, Nestor [UNIFESP]
dc.contributor.authorHooper, Cléber S
dc.contributor.authorAraújo-jorge, Tânia C De
dc.contributor.authorHenriques-pons, Andréa
dc.contributor.institutionInstituto Oswaldo Cruz-Fiocruz Laboratório de Biologia Celular
dc.contributor.institutionUniversidade Federal do Rio de Janeiro Instituto de Biofísica Carlos Chagas Filho
dc.contributor.institutionUniversidade Federal Fluminense Instituto Biomédico Departamento de Fisiologia e Farmacologia
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionCentro de Criação de Animais de Laboratório Departamento de Controle de Qualidade Animal
dc.date.accessioned2015-06-14T13:41:19Z
dc.date.available2015-06-14T13:41:19Z
dc.date.issued2009-12-01
dc.description.abstractTrypanosoma cruzi infection induces diverse alterations in immunocompetent cells and organs, myocarditis and congestive heart failure. However, the physiological network of disturbances imposed by the infection has not been addressed thoroughly. Regarding myocarditis induced by the infection, we observed in our previous work that Fas-L-/- mice (gld/gld) have very mild inflammatory infiltration when compared to BALB/c mice. However, all mice from both lineages die in the early acute phase. Therefore, in this work we studied the physiological connection relating arterial pressure, renal function/damage and cardiac insufficiency as causes of death. Our results show that a broader set of dysfunctions that could be classified as a cardio/anaemic/renal syndrome is more likely responsible for cardiac failure and death in both lineages. However, gld/gld mice had very early glomerular deposition of IgM and a more intense renal inflammatory response with reduced renal filtration, which is probably responsible for the premature death in the absence of significant myocarditis in gld/gld.en
dc.description.affiliationInstituto Oswaldo Cruz-Fiocruz Laboratório de Biologia Celular
dc.description.affiliationUniversidade Federal do Rio de Janeiro Instituto de Biofísica Carlos Chagas Filho
dc.description.affiliationUniversidade Federal Fluminense Instituto Biomédico Departamento de Fisiologia e Farmacologia
dc.description.affiliationUniversidade Federal de São Paulo (UNIFESP) Escola Paulista de Medicina Disciplina de Nefrologia
dc.description.affiliationCentro de Criação de Animais de Laboratório Departamento de Controle de Qualidade Animal
dc.description.affiliationUnifespUNIFESP, EPM, Disciplina de Nefrologia
dc.description.sourceSciELO
dc.format.extent1063-1071
dc.identifierhttp://dx.doi.org/10.1590/S0074-02762009000800002
dc.identifier.citationMemórias do Instituto Oswaldo Cruz. Instituto Oswaldo Cruz, Ministério da Saúde, v. 104, n. 8, p. 1063-1071, 2009.
dc.identifier.doi10.1590/S0074-02762009000800002
dc.identifier.fileS0074-02762009000800002.pdf
dc.identifier.issn0074-0276
dc.identifier.scieloS0074-02762009000800002
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/5401
dc.identifier.wosWOS:000274413300002
dc.language.isoeng
dc.publisherInstituto Oswaldo Cruz, Ministério da Saúde
dc.relation.ispartofMemórias do Instituto Oswaldo Cruz
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectTrypanosoma cruzien
dc.subjectFas-Len
dc.subjectmyocarditisen
dc.subjectacute kidney injuryen
dc.titleAbsence of Fas-L aggravates renal injury in acute Trypanosoma cruzi infectionen
dc.typeinfo:eu-repo/semantics/article
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