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Prepublished online as a Blood First Edition Paper on February 27, 2003; DOI 10.1182/blood-2002-12-3710.
Submitted December 5, 2002
Accepted January 22, 2003
Adhesion of normal and P. falciparum ring-infected erythrocytes to endothelial cells and the placenta involves the rhoptry-derived Ring Surface Protein-2
Jean Bernard Lekana Douki, Yvon Sterkers, Catherine Lepolard, Boubacar Traore, Fabio T M Costa, Artur Scherf, and Jurg Gysin*
Unite de Parasitologie Experimentale, Universite de la Mediterranee ( Aix-Marseille II), Marseille, France
Unite de biologie des Interactions Hote-Parasite, Institut Pasteur, Paris, France
* Corresponding author; email: gysin{at}medecine.univ-mrs.fr.
Recent findings have challenged the current view of Plasmodium falciparum blood-stage biology by demonstrating the cytoadhesion of early ring-stage infected erythrocytes (rIE) to host endothelial cells and placental syncytiotrophoblasts. The adhesion of rIE was only observed in parasites that bind to the placenta via chondroitin sulphate A (CSA). In this work, a panel of mouse monoclonal antibodies (mAbs) that specifically inhibit cytoadhesion of rIE but not of mature IE were generated. The previously described Ring Surface Protein 2 (RSP-2), a 42 kDa protein, was identified as the target of the ring-stage specific mAbs. Time course surface fluorescence experiments revealed a short-lived overlap (approx. 4 hours) of expression of RSP-2 and P. falciparum Erythrocyte Membrane Protein 1 (PfEMP1). Their consecutive expression enables IE to sequester to endothelial cells during the entire blood stage cycle. During this study, a novel adhesion phenotype was detected in parasite cultures, the adhesion of normal erythrocytes (nE) to endothelial cells. All adherent nE were coated with RSP-2. Immunolocalisation studies shows that RSP-2 is a rhoptry-derived protein, which is presumably discharged onto the erythrocyte membrane during contact with merozoites. Our results identify RSP-2 as a key molecule in sequestration of young blood stage forms and nE to endothelial cells.
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