Publication: Human vascular endothelial cell adhesion receptors for plasmoclium falciparum-infected erythrocytes: Roles for endothelial leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1
Issued Date
1992-10-01
Resource Type
ISSN
15409538
00221007
00221007
Other identifier(s)
2-s2.0-0026759659
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Journal of Experimental Medicine. Vol.176, No.4 (1992), 1183-1189
Suggested Citation
Christian F. Ockenhouse, Tatsuya Tegoshi, Yoshimasa Maeno, Christopher Benjamin, May Ho, Khin Ei Kan, Ye Thway, Kyan Win, Masamichi Aikawa, Roy R. Lobb Human vascular endothelial cell adhesion receptors for plasmoclium falciparum-infected erythrocytes: Roles for endothelial leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1. Journal of Experimental Medicine. Vol.176, No.4 (1992), 1183-1189. doi:10.1084/jem.176.4.1183 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/22293
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Title
Human vascular endothelial cell adhesion receptors for plasmoclium falciparum-infected erythrocytes: Roles for endothelial leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1
Abstract
The clinical complications associated with severe and cerebral malaria occur as a result of the intravascular mechanical obstruction of erythrocytes infected with the asexual stages of the parasite, Plasmodiumfakiparum. We now report that a primary P.fakiparum-infected erythrocyte (parasitized red blood cell [PRBC]) isolate from a patient with severe complicated malaria binds to cytokineinduced human vascular endothelial cells, and that this adhesion is in part mediated by endothelial leukocyte adhesion molecule 1 (ELAM-1) and vascular cell adhesion molecule 1 (VCAM-1). PRBC binding to tumor necrosis factor α (TNF-α-activated human vascular endothelial cells is partially inhibited by antibodies to ELAM-1 and ICAM-1 and the inhibitory effects of these antibodies is additive. PRBCs selected in vitro by sequential panning on purified adhesion molecules bind concurrently to recombinant soluble ELAM-1 and VCAM-1, and to two previously identified endothelial cell receptors for PRBCs, ICAM-1, and CD36. Post-mortem brain tissue from patients who died from cerebral malaria expressed multiple cell adhesion molecules including ELAM-1 and VCAM-1 on cerebral microvascular endothelium not expressed in brains of individuals who died from other causes. These results ascribe novel pathological functions for both ELAM-1 and VCAM-1 and may help delineate alternative adhesion pathways PRBCs use to modify malaria pathology. © 1992, Rockefeller University Press., All rights reserved.