Papel de citocinas e da leptina na imunopatologia da fase aguda na infecção experimental pelo trypanosoma cruzi em camundongos nocautes para IL-4 e IFN-γ

• Ano de defesa: 2017
• Autor(a) principal: Almeida, Vera Lucia Lima de
• Orientador(a): Machado, Juliana Reis
• Banca de defesa: Machado, Juliana Reis, Oliveira, Flávia Aparecida de, Castro, Ana Maria de
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Goiás
• Programa de Pós-Graduação: Programa de Pós-graduação em Medicina Tropical e Saúde Publica (IPTSP)
• Departamento: Instituto de Patologia Tropical e Saúde Pública - IPTSP (RG)
• País: Brasil
• Palavras-chave em Português: Trypanosoma cruzi; Resposta imune celular; Coração; Adipocitocinas; Nocaute
• Palavras-chave em Inglês: Cellular immune response; Heart; Adipocytokines; Knockouts
• Área do conhecimento CNPq: CIENCIAS DA SAUDE::MEDICINA
• Link de acesso: http://repositorio.bc.ufg.br/tede/handle/tede/7821

Chagas disease is a parasitic disease caused by the Protozoan Trypanosoma cruzi. Approximately 30% of infected individuals develop cardiac manifestations. Among the factors involved in this evolution highlights the role of inflammation. Evidence points to an important relationship of adipokines with the cellular immune response and inflammation. The present study is objective is to evaluate the role of cytokines and leptin on immunopathology of acute phase of experimental infection by T. cruzi. For this we used C57Bl/6 WT mice, C57Bl/6 WT KO IFN-γ, Balb-c WT and Balb-c KO IL-4 100 infected with of Colombian strain forms of T. cruzi and non-infected controls was analyzed in the hearts the presence of T. cruzi, fibrosis, inflammatory infiltrate, production of cytokines in situ and serum levels of leptin, TNF-α and IL-10. Noted greater tissue parasitism in C57Bl/6 animals KO IFN-γ, but no difference in the intensity of the inflammatory infiltrate and percentage of fibrosis. Regarding cytokines C57Bl/6 mice IFN-γ KO infected showed increased TNF-α in situ, as well as the Balbc KO IL-4. Despite greater expression in situ, systemically animals Balb-c KO IL-4 have shown to be good producers of TNF-α and IL-10 as well as the C57Bl/6 KO IFNγ. However, these last have shown to be good producers of serum leptin, as well as the Balb-c. Thus, our results indicate that in the absence of IFN-γ mice infected can' not control the tissue parasitism. However, feature increased in situ of TNF-α and serum leptin as a compensatory mechanism of the Th1 response deficiency.