Depletion of immune effector cells induces myocardial damage in the acute experimental Trypanosoma cruzi infection: ultrastructural study in rats.

The contribution of radiosensitive cells and macrophages to myocardial immunopathology has been studied in rats inoculated with Trypanosoma cruzi, Y strain. Immunodepression was induced by gamma irradiation and depletion of radioresistant macrophages was achieved by silica, a selective cytotoxic agent for macrophages. Irradiated or silica treated rats and age-matched controls were sacrificed at day 12 of infection so as to study the heart by light and electron microscopy. In the infected controls, damaged cardiomyocytes were directly related to tissue parasitism; inflammatory cells, predominantly lymphocytes and macrophages, were present. The drastic depletion of radiosensitive cells (lymphocytes and granulocytes), as well as the depletion of macrophages by silica, induced cardiomyocytes damage during the acute infection, exacerbating the lesions seen in the infected controls. In the irradiated-infected and silica treated-infected animals, degenerating cardiomyocytes, parasitized or not, were frequently observed, displaying evident signs of cytoplasmic and nuclear damage. Some signs of cardiomyocyte damage (irregular distribution of glycogen particles and myofibrils with shrinkage and aggregation of Z bands) were present only in silica treated-infected animals. The findings suggest that immune effector cells may not play a major role in the cardiomyocyte damage induced by acute. Chagas disease, arguing against the autoimmune etiology of Chagasic cardiomyopathy.