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https://www.arca.fiocruz.br/handle/icict/23209
Tipo de documento
ArtigoDireito Autoral
Acesso restrito
Data de embargo
2030-01-01
Coleções
- IOC - Artigos de Periódicos [12500]
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DEATH OF ADRENOCORTICAL CELLS DURING MURINE ACUTE T. CRUZI INFECTION IS NOT ASSOCIATED WITH TNF-R1 SIGNALING BUT MOSTLY WITH THE TYPE II PATHWAY OF FAS-MEDIATED APOPTOSIS
Glucocorticoid
Apoptosis
Trypanosoma cruzi
Tumor necrosis factor alpha
Fas
Trypanosoma cruzi
Glândulas Suprarrenais
Glucocorticoides
Antígenos CD95
Fator de Necrose Tumoral alfa
Autor(es)
Afiliação
Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología Clínica y Experimental de Rosario. Rosario, Argentina.
Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental. Rosario, Argentina.
Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología Clínica y Experimental de Rosario. Rosario, Argentina.
Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología Clínica y Experimental de Rosario. Rosario, Argentina.
Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología Clínica y Experimental de Rosario. Rosario, Argentina.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa sobre o Timo. Rio de Janeiro, RJ. Brasil.
Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental. Rosario, Argentina.
Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología Clínica y Experimental de Rosario. Rosario, Argentina.
Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental. Rosario, Argentina.
Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología Clínica y Experimental de Rosario. Rosario, Argentina.
Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología Clínica y Experimental de Rosario. Rosario, Argentina.
Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología Clínica y Experimental de Rosario. Rosario, Argentina.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Pesquisa sobre o Timo. Rio de Janeiro, RJ. Brasil.
Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Fisiología Experimental. Rosario, Argentina.
Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología Clínica y Experimental de Rosario. Rosario, Argentina.
Resumo em Inglês
Earlier studies from our laboratory demonstrated that acute experimental Trypanosoma cruzi infection promotes an intense inflammation along with a sepsis-like dysregulated adrenal response characterized by normal levels of ACTH with raised glucocorticoid secretion. Inflammation was also known to result in adrenal cell apoptosis, which in turn may influence HPA axis uncoupling. To explore factors and pathways which may be involved in the apoptosis of adrenal cells, together with its impact on the functionality of the gland, we carried out a series of studies in mice lacking death receptors, such as TNF-R1 (C57BL/6-(Tnfrsf1a tm1Imx) or TNF-R1(-/-)) or Fas ligand (C57BL/6 Fas-deficient lpr mice), undergoing acute T. cruzi infection. Here we demonstrate that the late hypercorticosterolism seen in C57BL/6 mice during acute T. cruzi infection coexists with and hyperplasia and hypertrophy of zona fasciculata, paralleled by increased number of apoptotic cells. Apoptosis seems to be mediated mainly by the type II pathway of Fas-mediated apoptosis, which engages the mitochondrial pathway of apoptosis triggering the cytochrome c release to increase caspase-3 activation. Fas-induced apoptosis of adrenocortical cells is also related with an exacerbated production of intra-adrenal cytokines that probably maintain the late supply of adrenal hormones during host response. Present results shed light on the molecular mechanisms dealing with these phenomena which are crucial not only for the development of interventions attempting to avoid adrenal dysfunction, but also for its wide occurrence in other infectious-based critical illnesses.
Palavras-chave
ApoptosisPalavras-chave em inglês
Adrenal glandsGlucocorticoid
Apoptosis
Trypanosoma cruzi
Tumor necrosis factor alpha
Fas
DeCS
ApoptosisTrypanosoma cruzi
Glândulas Suprarrenais
Glucocorticoides
Antígenos CD95
Fator de Necrose Tumoral alfa
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