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

Authors
Citation
Rcn. Melo, Depletion of immune effector cells induces myocardial damage in the acute experimental Trypanosoma cruzi infection: ultrastructural study in rats, TISSUE CELL, 31(3), 1999, pp. 281-290
Citations number
47
Categorie Soggetti
Cell & Developmental Biology
Journal title
TISSUE & CELL
ISSN journal
00408166 → ACNP
Volume
31
Issue
3
Year of publication
1999
Pages
281 - 290
Database
ISI
SICI code
0040-8166(199906)31:3<281:DOIECI>2.0.ZU;2-C
Abstract
The contribution of radiosensitive cells and macrophages to myocardial immu nopathology has been studied in rats inoculated with Trypanosoma cruzi, Y s train. Immunodepression was induced by gamma irradiation and depletion of r adioresistant macrophages was achieved by silica, a selective cytotoxic age nt for macrophages. Irradiated or silica treated rats and age-matched contr ols were sacrificed at day 12 of infection so as to study the heart by ligh t and electron microscopy. In the infected controls, damaged cardiomyocytes were directly related to tissue parasitism; inflammatory cells, predominan tly lymphocytes and macrophages, were present. The drastic depletion of rad iosensitive cells (lymphocytes and granulocytes), as well as the depletion of macrophages by silica, induced cardiomyocytes damage during the acute in fection, exacerbating the lesions seen in the infected controls. In the irr adiated-infected and silica treated-infected animals, degenerating cardiomy ocytes, parasitized or not, were frequently observed, displaying evident si gns 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 an imals, 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.