Key result
Trypanosoma cruzi infection in rats induces acute myositis and satellite cell-mediated regeneration without chronic fibrosis.
The study demonstrates that T. cruzi-induced myositis involves direct parasite-induced myofibre degeneration and subsequent regeneration, arguing against a primary autoimmune mechanism in both acute and chronic phases.
Challenges autoimmune primacy in experimental T. cruzi myositis; leaves open human translation.
Although Chagas' disease is known to provoke severe acute myositis, information on muscle regeneration is missing. The current paper shows that during T. cruzi infection in rats, skeletal muscle parasitism and the consequent inflammatory process are higher in muscle with a high proportion of type-I myofibres (soleus and diaphragm). Immunohistochemistry showed an acute inflammatory process characterized by ED1+ and ED2+ macrophages, CD8+ lymphocytes, and NK cells. Parasite-nest rupture provoked segmental degeneration of myofibres followed by regeneration. These phenomena were observed at both light and transmission electron microscopy levels. Myofibre regeneration involved activation of satellite cells assessed by the expression of MyoD, a muscle-specific transcription factor. Ultrastructural evidence of fusion of myoblast-like cells with the intact segment of degenerating fibres has been provided. At the chronic phase no signs of fibrosis were found, but sparse and small inflammatory foci were found. Our results argue against the relevant participation of autoimmunity phenomena in both acute and chronic phases and furnish a new view for explaining histopathological findings in human patient muscles.
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Maldonado et al. (2004) studied Trypanosoma cruzi-induced myositis. Trypanosoma cruzi infection was evaluated on Skeletal muscle parasitism, inflammation, and regeneration. Trypanosoma cruzi infection in rats induces acute myositis with segmental myofibre degeneration followed by satellite cell-mediated regeneration, without signs of fibrosis in the chronic phase.
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