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Blood, Vol. 96 No. 1 (July 1), 2000:
pp. 327-333
Sulfated glycoconjugates enhance CD36-dependent adhesion of
Plasmodium falciparum-infected erythrocytes to human
microvascular endothelial cells
Christopher John McCormick,
Christopher I. Newbold, and
Anthony R. Berendt
From the Adhesion and Infection Laboratory and the Molecular
Parasitology Group, Institute of Molecular Medicine, John Radcliffe
Hospital, Oxford, UK.
A novel adhesive pathway that enhances the adhesion of
Plasmodium falciparum-infected erythrocytes (IEs) to
endothelial cells has been identified. The sulfated glycoconjugates
heparin, fucoidan, dextran sulfate 5000, and dextran sulfate 500 000
caused a dramatic increase in adhesion of IEs to human dermal
microvascular endothelial cells. The same sulfated glycoconjugates had
little effect on IE adhesion to human umbilical vein endothelial cells,
a CD36-negative cell line. The effect was abolished by a monoclonal
antibody directed against CD36, suggesting that enhanced adhesion to
endothelium is dependent on CD36. No effect was observed on adhesion to
purified platelet CD36 cells immobilized on plastic. The same sulfated glycoconjugates enhanced adhesion of infected erythrocytes to COS cells
transfected with CD36, and this was inhibited by the CD36 monoclonal
antibody. These findings demonstrate a role for sulfated
glycoconjugates in endothelial adherence that may be important in
determining the location and magnitude of sequestration through
endogenous carbohydrates. In addition, they highlight possible
difficulties that may be encountered from the proposed use of sulfated
glycoconjugates as antiadhesive agents in patients with severe malaria.
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