Journal
EXPERIMENTAL PARASITOLOGY
Volume 97, Issue 1, Pages 15-23Publisher
ACADEMIC PRESS INC
DOI: 10.1006/expr.2000.4576
Keywords
Trypanosoma cruzi; Chagas disease; myocarditis; silica; macrophage depletion; macrophage activation; monocytes/macrophages; electron microscopy; macrophages and Trypanosoma cruzi infection in rats
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The contribution of mononuclear phagocytes to host resistance against acute Chagas disease has been studied in vivo in a rat model inoculated with Trypanosoma cruzi, Y strain. Acute T. cruzi infection triggered a dramatic increase (937%) in peripheral blood monocyte number at day 12 of infection. At this point, histological analysis of the heart showed high parasitism and diffuse and a moderate to intense mononuclear inflammatory process. Ultrastructural study revealed a large number of macrophages, in addition to lymphocytes and undifferentiated cells. Clusters of macrophages exhibited different morphological phenotypes, with evident signs of activation (increase in size, surface rufflings, and amount of cytoplasmic organelles). Cell-to-cell contacts involving macrophages and lymphocytes or macrophages and monocytes were observed. Depletion of macrophages by treatment with silica, a selective cytotoxic agent for these cells, caused a significant increase in the number of amastigote nests in cardiomyocytes. The present findings indicate that the early phase of infection with T. cruzi induces rapid production, maturation, and activation of the monocyte/macrophage system so as to control T. cruzi replication, emphasizing the crucial role for macrophages in the rat resistance to Chagas disease. (C) 2001 Academic Press.
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