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Regulatory effects of IL-18 on cytokine profiles and development of myocarditis during Trypanosoma cruzi infection.

Esper, Lísia; Utsch, Lara; Soriani, Frederico M; Brant, Fátima; Esteves Arantes, Rosa Maria; Campos, Camila F; Pinho, Vanessa; Souza, Danielle G; Teixeira, Mauro Martins; Tanowitz, Herbert Bernard; Vieira, Leda Quercia; Machado, Fabiana Simão.
Microbes Infect; 16(6): 481-90, 2014 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-24704475
Chagas disease, caused by Trypanosoma cruzi (Tc), is an important cause of heart disease. Resistance to Tc infection is multifactorial and associated with Th1 response. IL-18 plays an important role in regulation of IFN-γ production/development of Th1 response. However, the role of IL-18 in the setting of Tc infection remains unclear. Therefore, we investigated the role of IL-18 in the modulation of immune response and myocarditis in Tc infection. C57BL/6 and IL-18 KO mice were infected with Tc (Y or Colombian strain) and parasitemia, immune response and pathology were evaluated. Y strain infection of IL-18 KO did not alter any parameters when compared with C57BL/6 mice. However, during the acute phase (20 and 40 days post infection-dpi), Colombian strain infected-IL-18 KO mice displayed higher serum levels of IL-12 and IFN-γ, respectively, and at the chronic phase (100 dpi) an increase in splenic IFN-γ-producing CD4(+) and CD8(+) T memory cells. There was an IL-10, FOXP3 and CD4(+)CD25(+) cells reduction during acute infection in spleen. Additionally, there was a significant reduction in leukocyte infiltration and parasite load in myocardium of chronically infected IL-18 KO mice. Collectively, these data indicate that IL-18 contributes to the pathogenesis of Tc-induced myocarditis when infected with Colombian but not Y strain. These observations also underscore that parasite and host strain differences are important in evaluation of experimental Tc infection pathogenesis.
Selo DaSilva