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Intense inflammatory response and high mortality rate are associated with dystrophin reduction in Trypanosoma cruzi‐infected mice

Heart failure is an important cause of morbidity and mortality in both acute and chronic phases of Chagas' disease. Taking into account that the contractile machinery inside the myocyte must remain intimately connected with the membrane and extracellular matrix, association provided by the dystrophin glycoprotein complex (DGC), this study was carried out to test the hypothesis that acutely infected murine hearts present changes of dystrophin expression. C57Bl/6 mice were infected with Y strain of T. cruzi. Histological analyses, immunohistochemistry (IH) for T. cruzi, immunofluorescence staining and Western blot for dystrophin were performed. Parasitemia peak at day 9 and the mortality rate peaked on day 20. The inflammatory infiltrate was present at day 14 and peaked at day 20. The IH for T. cruzi showed parasite persistence up to 20 days pi and then it became rare. Dystrophin was focally reduced at day 14 and completely lost 20 days pi. A correlation between the amount of dystrophin and mortality rate was observed. The peak of mortality was correlated with the focal loss of dystrophin. Our results lend support to the hypothesis that changes in cytoskeletal proteins and, in particular, dystrophin could represent the partial loss of the mechanical binding of the entire array of myofibrils to the extracellular matrix, thus providing a final common pathway for contractile dysfunction in these mice.