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Thrombospondin mediates the cytoadherence of Plasmodium falciparum-
infected red cells to vascular endothelium in shear flow conditions
EP Rock, EF Roth , RR Rojas-Corona, JA Sherwood, RL Nagel, RJ Howard and DK Kaul
Howard Hughes Medical Institute, Bethesda, MD.
Cerebral malaria is thought to involve specific attachment of Plasmodium
falciparum-infected knobby red cells to venular endothelium. The nature of
surface ligands on host endothelial cells that may mediate cytoadherence is
poorly understood. We have investigated the effects of soluble
thrombospondin, rabbit antiserum raised against thrombospondin, and human
immune serum on cytoadherence of parasitized erythrocytes in ex vivo
mesocecum vasculature. Preincubation of infected red cells with soluble
thrombospondin or human immune serum inhibits binding of infected red cells
to rat venular endothelium. Infusion of the microcirculatory preparation
with rabbit antithrombospondin antibodies before perfusion of parasitized
erythrocytes also resulted in decreased cytoadherence. In addition,
incubation of infected cells with human immune sera obtained from malaria
patients significantly inhibited the observed cytoadherence. Our results
indicate that thrombospondin mediates binding of infected red cells to
venular endothelium and may thus be involved in the pathogenesis of
cerebral malaria.
Volume 71,
Issue 1,
pp. 71-75,
01/01/1988
Copyright © 1988 by The American Society of Hematology
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