PLASMODIUM-FALCIPARUM - CHARACTERIZATION OF ADHESION OF FLOWING PARASITIZED RED-BLOOD-CELLS TO PLATELETS

Adhesion of parasitized red blood cells to vascular endothelium contri butes to the ischaemic pathology of severe falciparum malaria. One of the endothelial cytoadhesion receptors, CD36, is also expressed by pla telets. We have studied adhesion of flowing parasitized cells to a sur face coated with immobilized, activated platelets, both as a model for CD36-mediated adhesion and because interaction with platelets might p lay a direct role in thrombotic complications of malaria. Parasitized cells were able to bind firmly to platelets over a range of shear stre ss (up to 0.3 Pa) close to those found in the microcirculation. The bi nding was largely abolished by treatment of platelets with antibody to CD36, with only a small effect by antibody to ICAM-1. Binding showed pH sensitivity consistent with previous reports of CD36-mediated cytoa dhesion. Fixation of the platelet surface with formaldehyde preserved adhesion and its antibody sensitivity to antibody against ICAM-1. Thus CD36-mediated binding is inhibited by glutaraldehyde-but not formalde hyde-fixation, while ICAM-1 can mediate adhesion after either form of fixation. We conclude that platelet-coated surfaces (with or without f ixation) represent a practically simple model for studying malarial cy toadhesion and that platelets are likely to be able to bind parasitize d cells in vivo and could thus promote vascular occlusion. (C) 1995 Ac ademic Press, Inc.