Abstract
Chagas disease, caused by the protozoan Trypanosoma cruzi, represents a serious health public problem with around seven million infected people worldwide. Approximately 30% of infected individuals will develop cardiac disorders during the chronic phase. However, the pathogenesis of Chagas disease remain incompletely elucidated with fundamental questions partially unanswered as the factors that lead to the development of clinical manifestations. Thereby, this study aims to investigate the importance of the association of T. cruzi strain, host sex, host immunological factors and changes in heart tissue in the progression of cardiac lesions in experimental Chagas disease. For this, 60 BALB/c mice were divided into three groups according to the T. cruzi strain (discrete typing unit TcI, TcII and TcVI). They were analyzed in acute phase (30 days pos‐infection ‐ 30dpi) and chronic phase (90 dpi). Ten uninfected mice formed the control group. Each group were formed by five males and five females. After the experimental period, mice were euthanized and blood and heart were collected. Anti‐T cruzi antibody and anti‐cardiac tissue antibody production were evaluated by ELISA. Parasite load in the heart was determined by qPCR. Histopathological analysis of heart was also performed. Most of the animals produced anti‐T. cruzi IgM antibody in the acute phase, whereas all mice were seropositive for IgG in chronic phase. TcI was characterized by elevated antibody levels with autoantibodies titers against the heart in chronic phase significantly higher than the other groups. Besides that TcI presented a greater number of parasites both in acute and chronic phase as well as more damage in heart tissue. No difference was observed between males and females. Amastigote nests were seen in mice analyzed in acute phase in TcI and TcVI, but not in TcII. The results confirm the participation of autoimmune response in chronic Chagas disease, which varies according to T. cruzi strain. It seems that the TcI was the most aggressive. However, the relationship between the studied factors and the severity of disease has not been established.Support or Funding InformationThis study was financed by Fundação de Apoio a Pesquisa do Distrito Federal (FAPDF), Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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