Intercellular adhesion molecule-1 and CD36 synergize to mediate adherence of Plasmodium falciparum-infected erythrocytes to cultured human microvascular endothelial cells.

Abstract

We have compared the adhesion of Plasmodium falciparum -infected erythrocytes to human dermal microvascular endothelial cells (HDMEC) and human umbilical vein endothelial cells (HUVEC) and have assessed the relative roles of the receptors CD36 and intercellular adhesion molecule-1 (ICAM-1). HUVEC (a cell line that expresses high levels of ICAM-1 but no CD36) mediate low levels of adhesion, whereas HDMEC (which constitutively express CD36) mediate high levels of adhesion even before ICAM-1 induction. ICAM-1 expression leads to yet greater levels of adhesion, which are inhibited both by anti-ICAM-1 and CD36 mAbs, despite no increase in the expression of CD36. The results indicate the presence of a substantial population of infected cells that require the presence of both receptors to establish adhesion. Synergy between these receptors could be demonstrated using a number of parasite lines, but it could not be predicted from the binding of these same parasite lines to purified ICAM-1 and CD36. This phenomenon could not be reproduced using either purified receptors presented on plastic, or formalin-fixed HDMEC, suggesting that receptor mobility is important. This is the first study to demonstrate receptor synergy in malaria cytoadherence to human endothelial cells, a phenomenon necessary for parasite survival and associated with disease severity. ( J. Clin.

Bacterial fibronectin-binding proteins and endothelial cell surface fibronectin mediate adherence of Staphylococcus aureus to resting human endothelial cells

“…Fibronectin, through its known interactions with integrin receptors present on endothelium (Albelda et al, 1989), is an ideal candidate molecule to orchestrate these events. Many other invasive pathogens use integrins as cellular receptors (for review see Berendt & McCormick, 1997) and Streptococcus pyogenes has already been shown to invade a number of epithelial cell lines through the interaction between fibronectin and epithelial-cell-surface integrins (Ozeri et al, 1998). Our observations thus prompt the speculation that S. aureus invades endothelial cells through similar mechanisms.…”

“…The relevant activation status of the endothelial cells in vivo is unknown and their phenotype will vary according to site. We previously showed that there are important differences between microvascular and large vessel endothelium in the expression and function of host receptors for the adhesion of malaria-infected erythrocytes (McCormick et al, 1997). Furthermore, for adhesion of both leukocytes and malaria-infected erythrocytes, endothelial receptors show differential adhesion under shear flow conditions, with ' rolling ' and ' static ' receptors.…”

Identification of a Plasmodium falciparum intercellular adhesion molecule-1 binding domain: A parasite adhesion trait implicated in cerebral malaria

“…A4tres-infected erythrocytes bind both ICAM-1 and CD36. These two proteins have been shown to synergize in mediating infected erythrocyte adhesion to cell lines that express both of these molecules (31). A CD36 binding domain has previously been shown to reside in the CIDR domain of PfEMP1 that bind CD36 (20,21).…”

Thrombospondin-1 Inhibits Nitric Oxide Signaling via CD36 by Inhibiting Myristic Acid Uptake

“…The activities of some TSP1 receptors differ between large vessel and microvascular endothelial cells, and some are regulated by specific contextual signals (4 -6). CD36, a member of the scavenger receptor B family, is a TSP1 receptor that is selectively expressed in microvascular endothelium (7,8). CD36 was initially reported to recognize CSVTCG sequences in the type 1 repeats of TSP1 (9), but further studies identified higher affinity binding to the adjacent GVQXR sequences in the second and third type 1 repeats (10, 11).…”