Intermembrane lipid transfer during Trypanosoma cruzi-induced erythrocyte membrane destabilization.

The ability of Trypanosoma cruzi to induce erythrocyte membrane destabilization in vitro was studied. Epimastigote forms adhered to human erythrocytes and caused fusion or lysis of the red cells, depending on the conditions of the interaction. Red cells were fused in the presence of calcium, while haemolysis was induced in the absence of the cation. Dextran 60 C facilitated fusion but delayed lysis. Optimum pH and temperature for fusion were 7.4 and 37 degrees C, respectively. Lipid alterations were produced in the plasma membrane of the red cell during the interaction with the parasite. A Ca(2+)-independent increase of lysophospholipids and free fatty acids was common to both the lysis and fusion processes. A relative increase of 1,2-diacylglycerides was unique to the fusion process and these changes were dependent on Ca2+. The transfer of free fatty acids and lysophospholipids from T. cruzi to erythrocyte membranes was demonstrated using parasites pre-labelled with radioactive phospholipids. Pre-treatment of parasites with exogenous phospholipase A2 abolished the fusogenicity, while lysis was increased. Neither fusion nor haemolysis occurred when the parasites were pre-treated with fatty acid free albumin, phospholipase A2 inhibitors or when these compounds were present in the medium during the parasite-erythrocyte interaction. Our results suggest that T. cruzi induces erythrocyte membrane destabilization in vitro by transfer of lipid material in a calcium independent manner and that this ion is necessary for other membrane alterations that lead to erythrocyte fusion.