TRYPANOSOMA-CRUZI RECOGNITION BY MACROPHAGES AND MUSCLE-CELLS - PERSPECTIVES AFTER A 15-YEAR STUDY

Macrophages and muscle cells are the main targets for invasion of Tryp anosoma cruzi. Ultrastructural studies of this phenomenon in vitro sho wed that invasion occurs by endocytosis, with attachment and internali zation being mediated by different components capable of recognizing e pi- or trypomastigotes (TRY). A parasitophorus vacuole was formed in b oth cell types, thereafter fusing with lysosomes. Then, the mechanism of T. cruzi invasion of host cells (HC) is essentially similar (during a primary infection in the absence of a specific immune response), re gardless of whether the target cell is a professional or a non-profess ional phagocytic cell. Using sugars, lectins, glycosidases, proteinase s and proteinase inhibitors, we observed that the relative balance bet ween exposed sialic acid and galactose/N-acetyl galactosamine (GAL) re sidues on the TRY surface, determines the parasite's capacity to invad e HC, and that lectin-mediated phagocytosis with GAL specificity is im portant for internalization of T. cruzi into macrophages. On the other hand, GAL on the surface of heart muscle cells participate on TRY adh esion. TRY need to process proteolytically both the HC and their own s urface, to expose the necessary ligands and receptors that allow bindi ng to, and internalization in the host cell. The diverse range of mole cular mechanisms which the parasite could use to invade the host cell may correspond to differences in the available ''receptors'' on the su rface of each specific cell type. Acute phase components, with lectin or proteinase inhibitory activities (alpha-macroglobulins), may also b e involved in T. cruzi-host cell interaction.