Absence of Fas-L aggravates renal injury in acute Trypanosoma cruzi infection
Trypanosoma 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.
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Instituto Oswaldo Cruz, Ministério da Saúde
2009
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oai:scielo:S0074-027620090008000022010-02-22Absence of Fas-L aggravates renal injury in acute Trypanosoma cruzi infectionOliveira,Gabriel Melo deMasuda,Masako OyaRocha,Nazaré NSchor,NestorHooper,Cléber SAraújo-Jorge,Tânia C deHenriques-Pons,Andréa Trypanosoma cruzi Fas-L myocarditis acute kidney injury Trypanosoma 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.info:eu-repo/semantics/openAccessInstituto Oswaldo Cruz, Ministério da SaúdeMemórias do Instituto Oswaldo Cruz v.104 n.8 20092009-12-01info:eu-repo/semantics/articletext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0074-02762009000800002en10.1590/S0074-02762009000800002 |
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Oliveira,Gabriel Melo de Masuda,Masako Oya Rocha,Nazaré N Schor,Nestor Hooper,Cléber S Araújo-Jorge,Tânia C de Henriques-Pons,Andréa |
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Oliveira,Gabriel Melo de Masuda,Masako Oya Rocha,Nazaré N Schor,Nestor Hooper,Cléber S Araújo-Jorge,Tânia C de Henriques-Pons,Andréa Absence of Fas-L aggravates renal injury in acute Trypanosoma cruzi infection |
author_facet |
Oliveira,Gabriel Melo de Masuda,Masako Oya Rocha,Nazaré N Schor,Nestor Hooper,Cléber S Araújo-Jorge,Tânia C de Henriques-Pons,Andréa |
author_sort |
Oliveira,Gabriel Melo de |
title |
Absence of Fas-L aggravates renal injury in acute Trypanosoma cruzi infection |
title_short |
Absence of Fas-L aggravates renal injury in acute Trypanosoma cruzi infection |
title_full |
Absence of Fas-L aggravates renal injury in acute Trypanosoma cruzi infection |
title_fullStr |
Absence of Fas-L aggravates renal injury in acute Trypanosoma cruzi infection |
title_full_unstemmed |
Absence of Fas-L aggravates renal injury in acute Trypanosoma cruzi infection |
title_sort |
absence of fas-l aggravates renal injury in acute trypanosoma cruzi infection |
description |
Trypanosoma 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. |
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Instituto Oswaldo Cruz, Ministério da Saúde |
publishDate |
2009 |
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http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0074-02762009000800002 |
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