Navegando por Palavras-chave "Fas-L"
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- ItemAcesso aberto (Open Access)Absence of Fas-L aggravates renal injury in acute Trypanosoma cruzi infection(Instituto Oswaldo Cruz, Ministério da Saúde, 2009-12-01) Oliveira, Gabriel Melo De; Masuda, Masako Oya; Rocha, Nazaré N; Schor, Nestor [UNIFESP]; Hooper, Cléber S; Araújo-jorge, Tânia C De; Henriques-pons, Andréa; Instituto Oswaldo Cruz-Fiocruz Laboratório de Biologia Celular; Universidade Federal do Rio de Janeiro Instituto de Biofísica Carlos Chagas Filho; Universidade Federal Fluminense Instituto Biomédico Departamento de Fisiologia e Farmacologia; Universidade Federal de São Paulo (UNIFESP); Centro de Criação de Animais de Laboratório Departamento de Controle de Qualidade AnimalTrypanosoma 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.