Immunopathological aspects of experimental Trypanosoma cruzi infection: correlation of immune complexes and other serological features with muscle lesions during the infection.
The pathogenesis of the tissue lesions observed in American trypanosomiasis (Chagas' disease) seems to depend on a variety of mechanisms. The present study was dedicated to the investigation of the evolution of muscle lesions and its relationship with immunological and parasitological parameters. Mice were infected i.p. with 10(5) blood forms of Trypanosoma cruzi (Columbian strain). A progressive increase in parasitaemia was observed which correlated with an increase in serum levels of IgG and IgM Trypanosoma-specific antibodies. Immune complex like material was detected in the serum (125I-C1q binding assay) on day 8 and reached maximum level between day 21 and 28. A concomitant fall in C3 levels was also observed. Inflammatory lesions and parasites were first observed in the striated muscle 2 weeks after infection. The cellular infiltrates involved macrophages and lymphoid cells; later on (week 3 onwards), intense necrosis appears and at the same time immunoglobulin and complement deposition were observed. These observations may indicate that, in addition to the cellular immune response, humoral mechanisms could contribute to the worsening of tissue lesions.
D000818:Animals; D000936:Antigen-Antibody Complex / Q000378:metabolism*; D000953:Antigens, Protozoan / Q000276:immunology; D014355:Chagas Disease / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D007111:Immunity, Cellular; D008297:Male; D051379:Mice; D009132:Muscles / Q000276:immunology* / Q000473:pathology; D013997:Time Factors; D014349:Trypanosoma cruzi / Q000276:immunology
D000936:Antigen-Antibody Complex; D000953:Antigens, Protozoan