Key result
Trypanosoma cruzi infection in CBA-J mice induced distinct cytokine patterns and cellular infiltrates associated with myocardial pathology, mimicking chronic human Chagas' heart pathology.
Local cytokine production patterns in the hearts of T. cruzi-infected CBA mice reflect the establishment of myocardial pathology, mimicking chronic human Chagas' heart disease.
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Supports CBA-J mice as model for Chagas cardiomyopathy research; leaves open translation of cytokine patterns to human therapies.
The authors analysed cytokine production in hearts of Trypanosoma cruzi-infected CBA-J mice by in situ immunocytochemical staining. Cellular infiltrates were recorded in hearts from both acute and chronic stages, but were not apparent in control hearts. In the acute heart, CD8 cells predominated, with associated production of IL-4, IL-6 and TNF-alpha. Cytokine production was characterized by IL-4, IL-5, IL-6 and TNF-alpha in the chronic heart, and numbers of CD4 and CD8 cells were more equal. At this stage, calcified infarctions and associated fibrosis were apparent, mimicking chronic human Chagas' heart pathology. The authors consider the CBA mouse an appropriate model of chronic T. cruzi infection, and suggest that local cytokine production reflects establishment of heart pathology.
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Sunnemark et al. (1996) studied Trypanosoma cruzi infection. Trypanosoma cruzi infection vs. Uninfected control hearts was evaluated on Cytokine production and cellular infiltrates in the heart. Trypanosoma cruzi infection in CBA-J mice induced distinct cytokine patterns and cellular infiltrates associated with myocardial pathology, mimicking chronic human Chagas' heart pathology.
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