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To investigate the possibility that cell contact could initiate a series of signals in both the host cell and the flagellate protozoan Trypanosoma cruzi, we studied [32P]-phospholipid turnover during parasite interaction with cellular membranes in vitro. Lipid alterations were produced in the parasite during the initial period of contact with the plasma membranes of human erythrocytes. In the presence of calcium an increment in phosphatidylethanolamine was observed with a concomitant decrease in phosphatidic acid fractions, whereas these modifications were not observed in the absence of calcium. There was an evident decrease in phosphatidylcholine and a shift in the phosphatidylinositol/lysophosphatidylethanolamine fraction among the phospholipids of major turnover in the absence or presence of calcium. Among the minor labeled species, lysophosphatidylcholine reached levels that duplicated control values, whereas the amounts of lysophosphatidylinositol, phosphatidylinositol 4-phosphate, and phosphatidylinositol 4,5-bisphosphate diminished by over 50%. All of these variations indicate that the parasite's contact with plasma membranes induces changes involving T. cruzi phospholipids and suggest the participation of these compounds in the activation of intracellular mechanisms that might be important during the life cycle of this parasite.

Ganglioside treatment of mice during their acute infection with Trypanosoma cruzi promoted long-term survival and clearance of parasites from the bloodstream and organs. Additionally, such treatment completely prevented the clinical manifestations of the infection, and progression into the chronic stages of the disease, for at least 18 months post-infection. Trypanosoma cruzi must invade nucleated cells to survive and reproduce within the mammalian host, and it has been suggested that ganglioside treatment inhibits the parasite's phospholipase A2 enzymes (PLA2), which are involved in membrane destabilization. However, since total brain gangliosides were not toxic to the parasite, either in xenic or axenic cultures, it seems unlikely that their action in vivo relates to their inhibition of PLA2. Other possible mechanisms of action are discussed.