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Blood, 15 September 2000, Vol. 96, No. 6, pp. 2292-2298
RED CELLS
Synergism of multiple adhesion molecules in mediating
cytoadherence of Plasmodium falciparum-infected
erythrocytes to microvascular endothelial cells under flow
Bryan G. Yipp,
Samantha Anand,
Tineke Schollaardt,
Kamala D. Patel,
Sornchai Looareesuwan, and
May Ho
From the Department of Microbiology and Infectious
Diseases, and the Immunology Research Group, University of Calgary,
Alberta, Canada; and the Faculty of Tropical Medicine, Mahidol
University, Bangkok, Thailand.
Plasmodium falciparum-infected erythrocytes (IRBCs)
have been shown to interact with a number of endothelial adhesion
molecules expressed on transfectants, on cell lines, and as immobilized purified receptor proteins under flow conditions. However, the experiments were designed in such a way that maximal numbers of adhesion molecules were provided as substratum. Whether the interactive events actually occur on microvascular endothelium, where the distribution and expression of adhesion molecules may be less, remains
undetermined. In this study, the cytoadherance of IRBCs on human dermal
microvascular endothelial cells (HDMECs) as a model of human
microvasculature was examined. IRBCs were observed to tether, roll, and
adhere on resting HDMECs, which constitutively expressed CD36 and
intercellular adhesion molecule-1 (ICAM-1) at an optimal shear stress
of 1 dyne/cm2. Stimulation of HDMECs with tumor necrosis
factor- for 5 and 24 hours, which resulted in up-regulation of
ICAM-1 and induction of vascular cell adhesion molecule-1 expression,
significantly increased the percentage of rolling cells that adhered
without affecting the rolling flux. In contrast, P-selectin expression on HDMECs induced by oncostatin M led to an increase in both rolling flux and adhesion. Inhibition studies with receptor-specific monoclonal antibodies revealed that adhesion of IRBCs on HDMECs was largely CD36
dependent, whereas rolling could be mediated by any of the adhesion
molecules studied. Collectively, these findings indicate that IRBCs
interact synergistically with multiple adhesion molecules on vascular
endothelium. The rolling of IRBCs may be the rate-limiting step in
cytoadherance, since it can be modulated by cytokines to enhance
CD36-mediated IRBC adhesion.
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