Immunopathological aspects of experimental Trypanosoma cruzi infection: correlation of immune complexes and other serological features with muscle lesions during the infection

Abstract

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.

Kinetics of Trypanosoma cruzi destruction in the mouse spleen

“…E v e n t u a l d i s i n t e g r a t i o n o f p a r a s i t i z e d macrophages occurring before the episode of massive cell destruction may depend on a different pathogenesis, since the host reaction was then limited to a focal infiltration by polymorphonuclear leukocytes. Similar findings observed in the connective tissue of mice have been correlated with local antigen-antibody reaction and hypocomplementemia 12 .…”

Immunopathology of Chagas disease

“…Presence of immuno-globulin and complement can be demonstrated in these focal lesions by immunofluorescence, revealing the early participation of humoral immune factors in pathogenesis (Silva et al 1985). Initially focal reactions are seen scattered distributed throughout the myocardium a few days after experimental inoculation.…”

The Classical Activation Pathway of the Human Complement System Is Specifically Inhibited by Calreticulin from Trypanosoma cruzi

“…Thus, TcCRT interference with C1q functions could alter immune complex processing with likely consequences in the pathogenesis of Chagas' disease (63)(64)(65)(66).…”