Key result
Acute T. cruzi infection in hamsters caused acute-phase signs in 50% of animals, which was associated with significantly increased cardiac parasitism and inflammatory cytokine expression.
Distinct outcomes of acute T. cruzi infection in hamsters are related to cardiac parasitism, cytokine expression, and changes in structural and stress response proteins.
Supports mechanistic insights into acute Chagas myocarditis from hamster data; leaves open clinical translation pending human studies.
BACKGROUND: Trypanosoma cruzi-infected outbred hamsters reproduce the range of different outcomes of Chagas disease noted in humans. We tested whether myocarditis, its mediators, and myocardial protein expression are related to the severity of the acute phase of T. cruzi infection in the hamster model. METHODS: Myocardium left ventricles (LVs) obtained from Syrian hamsters infected with T. cruzi were collected 21 days after infection. Myocarditis and the T. cruzi nest/antigen area were analyzed by histological and morphometric analysis. Cytokine and chemokine messenger RNA (mRNA) expression was analyzed using real-time reverse-transcriptase polymerase chain reaction. Differentially expressed proteins were identified by 2-dimensional electrophoresis, followed by mass spectrometry. RESULTS: While in the acute phase of infection, 50% of animals displayed weight loss and signs of acute-phase infection (hereafter referred to as "acute-phase signs" [APS]) (e.g., lethargy, vomiting, and diarrhea). Both the T. cruzi nest/antigen area and the expression of interferon-gamma, tumor necrosis factor-alpha, interleukin-10, and CCL3 mRNA were significantly increased in the LVs of animals with APS, compared with the LVs of animals without APS. Animals with APS, those without APS, and uninfected animals demonstrated distinct myocardial expression of contractile, stress response, and metabolism proteins. CONCLUSIONS: The distinct outcomes of acute T. cruzi infection in Syrian hamsters are related to cardiac parasitism, cytokine expression, and changes in the expression of structural/contractile and stress response proteins that may be associated with alterations in the cardiomyocyte cytoskeleton.
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Bilate et al. (2008) studied Trypanosoma cruzi infection. Trypanosoma cruzi infection vs. Uninfected animals or infected animals without acute-phase signs was evaluated on Myocarditis, T. cruzi nest/antigen area, cytokine/chemokine mRNA expression, and protein expression. Acute T. cruzi infection in hamsters caused acute-phase signs in 50% of animals, which was associated with significantly increased cardiac parasitism and inflammatory cytokine expression.
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