Sulfated glycoconjugates enhance CD36-dependent adhesion of Plasmodium falciparum-infected erythrocytes to human microvascular endothelial cells

A novel adhesive pathway that enhances the adhesion of Plasmodium falciparu m-infected erythrocytes (IEs) to endothelial cells has been identified. The sulfated glycoconjugates heparin, fucoidan, dextran sulfate 5000, and dext ran sulfate 500 000 caused a dramatic increase in adhesion of IEs to human dermal microvascular endothelial cells. The same sulfated glycoconjugates h ad little effect on IE adhesion to human umbilical vein endothelial cells, a CD36-negative cell line. The effect was abolished by a monoclonal antibod y directed against CD36, suggesting that enhanced adhesion to endothelium i s dependent on CD36, No effect was observed on adhesion to purified platele t CD36 cells immobilized on plastic. The same sulfated glycoconjugates enha nced adhesion of infected erythrocytes to COS cells transfected with CD36, and this was inhibited by the CD36 monoclonal antibody. These findings demo nstrate a role for sulfated glycoconjugates in endothelial adherence that m ay be important in determining the location and magnitude of sequestration through endogenous carbohydrates. In addition, they highlight possible diff iculties that may be encountered from the proposed use of sulfated glycocon jugates as antiadhesive agents in patients with severe malaria. (Blood, 200 0;96:327-333) (C) 2000 by The American Society of Hematology.