Mechanisms of invasion and replication of the intracellular stage in Trypanosoma cruzi.
Amastigotes obtained from spleens of mice infected with different strains of Trypanosoma cruzi were examined for their ability to invade macrophages and L929 cells and to initiate infection in mice. Both types of cells were readily invaded by organisms of the strains Y, MR, and Tulahuen. Organisms of the CL strain were taken up by both types of cells at a rate that was significantly lower than that for organisms of the other strains. However, all strains multiplied intracellularly. Activated macrophages inhibited the replication of intracellular organisms. Treatment of normal macrophages with cytochalasin B, trypsin, chymotrypsin, or pronase significantly inhibited phagocytosis, but the inhibitory effect was reversible. Mice injected with spleen amastigotes developed parasitemia and died of the infection. These results demonstrate that spleen amastigotes are able to infect, survive, and replicate within professional and nonprofessional phagocytes and to initiate infection in vivo. Interiorization of spleen amastigotes is by phagocytosis and is dependent upon a protease-sensitive receptor(s) on the cell surfaces of host macrophages.
D000818:Animals; D002478:Cells, Cultured; D014355:Chagas Disease / Q000469:parasitology*; D003571:Cytochalasin B / Q000494:pharmacology; D005260:Female; D005347:Fibroblasts / Q000469:parasitology; D008264:Macrophages / Q000469:parasitology; D051379:Mice; D010447:Peptide Hydrolases; D010587:Phagocytosis / Q000187:drug effects; D014349:Trypanosoma cruzi / Q000254:growth & development*
D003571:Cytochalasin B; D010447:Peptide Hydrolases