IPTSP - Instituto de Patologia Tropical e Saúde Pública
URI Permanente desta comunidade
Navegar
Navegando IPTSP - Instituto de Patologia Tropical e Saúde Pública por Autor "Almeida, Vera Lucia Lima de"
Agora exibindo 1 - 1 de 1
Resultados por página
Opções de Ordenação
Item 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(Universidade Federal de Goiás, 2017-04-07) Almeida, Vera Lucia Lima de; Lino Júnior, Ruy de Souza; Celes, Mara Rúbia Nunes; http://lattes.cnpq.br/1234213665964187; Machado, Juliana Reis; http://lattes.cnpq.br/5289363102869037; Machado, Juliana Reis; Oliveira, Flávia Aparecida de; Castro, Ana Maria deChagas 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.