Parasitization of mesenchymal cells by Trypanosoma cruzi results in the elaboration of a fibroblast-stimulating factor, which may initiate myocardial fibrosis in Chagasic cardiomyopathy.
Suggests a parasite-derived factor may drive fibrosis in Chagas disease; leaves open its contribution to human cardiomyopathy progression.
Myocardial fibrosis can occur as a complication of chronic infection of the heart with Trypanosoma cruzi (Chagas' disease) and can lead to serious disability. To assess whether there might be a direct relationship between intracellular parasitization and subsequent tissue fibrosis in this disease, we tested serum-free conditioned media from cultures of fibroblasts, vascular smooth-muscle cells, and myocardial cells for fibroblast-stimulating activity. Conditioned media from all infected cultures, but not from uninfected cultures, stimulated fibroblast [3H]thymidine incorporation, DNA and protein synthesis, and cell proliferation. Fibroblast-stimulating activity was also detected in extracts of amastigotes but not of trypomastigotes or epimastigotes. We conclude that parasitization of mesenchymal cells, including myocardial cells, results in elaboration of a fibroblast-stimulating factor(s), perhaps of parasite origin. We postulate that this factor may play a role in initiation of myocardial fibrosis in Chagas' disease.
No takes yet. Share an insight, caveat, or question.
Wyler et al. (1987) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: