Plasmodium falciparum Uses gC1qR/HABP1/p32 as a Receptor to Bind to Vascular Endothelium and for Platelet-Mediated Clumping

PLoS Pathogens

Kasturi Datta¹  Bhaswati Banerjee²  Anup Kumar Biswas²  Kwang Sik Kim³  Abdul Hafiz³  Chetan E Chitnis³ 

[1] Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America;Malaria Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, India;School of Environmental Sciences, Jawaharlal Nehru University, New Delhi, India

关键词: Plasmodium;    Platelets;    Cell binding assay;    Endothelial cells;    Cell binding;    Malaria;    Endothelium;    Receptor binding assays;   

DOI  :  10.1371/journal.ppat.0030130

学科分类：生物科学（综合）

来源: Public Library of Science

【 摘 要 】

The ability of Plasmodium falciparum–infected red blood cells (IRBCs) to bind to vascular endothelium, thus enabling sequestration in vital host organs, is an important pathogenic mechanism in malaria. Adhesion of P. falciparum IRBCs to platelets, which results in the formation of IRBC clumps, is another cytoadherence phenomenon that is associated with severe disease. Here, we have used in vitro cytoadherence assays to demonstrate, to our knowledge for the first time, that P. falciparum IRBCs use the 32-kDa human protein gC1qR/HABP1/p32 as a receptor to bind to human brain microvascular endothelial cells. In addition, we show that P. falciparum IRBCs can also bind to gC1qR/HABP1/p32 on platelets to form clumps. Our study has thus identified a novel host receptor that is used for both adhesion to vascular endothelium and platelet-mediated clumping. Given the association of adhesion to vascular endothelium and platelet-mediated clumping with severe disease, adhesion to gC1qR/HABP1/p32 by P. falciparum IRBCs may play an important role in malaria pathogenesis.

【 授权许可】

CC BY