title: Adherence of Plasmodium falciparum-infected erythrocytes to chondroitin 4-sulfate.
abstract: Adherence of Plasmodium falciparum-infected erythrocytes (PRBCs) to the microvascular endothelium of specific organs and consequent sequestration is believed to be responsible for the development of malaria pathology. A number of studies have shown that cell adhesion molecules expressed on the surface of endothelial cells mediate the adherence. Recent studies indicate that a subpopulation of PRBCs adhere to chondroitin 4-sulfate (C4S). This adhesion can be effectively inhibited by C4S oligosaccharides. In pregnant women, the placenta specifically selects C4S-adherent PRBCs, and thus these phenotypes multiply and sequester in the intervillous spaces. Over successive pregnancies, women develop a protective humoral response to the C4S-adhesion phenotype. Disruption of C4S-mediated PRBCs adhesion using either a C4S oligosaccharide mimetic or an antiC4S-adhesion vaccine can be an efficient strategy for the treatment of malaria caused by C4S-adherent P. falciparum.
authors.affiliation: Department of Biochemistry and Molecular Biology, Georgetown University Medical Center, Washington, DC 20007, USA. gowda@bc.georgetown.edu
authors.forename: D C
authors.initials: DC
authors.lastname: Gowda
authors.forename: C F
authors.initials: CF
authors.lastname: Ockenhouse
mesh_terms: D000818:Animals; D000953:Antigens, Protozoan / Q000378:metabolism; D002240:Carbohydrate Sequence; D002448:Cell Adhesion; D002809:Chondroitin Sulfates / Q000378:metabolism*; D004912:Erythrocytes / Q000378:metabolism / Q000469:parasitology*; D005260:Female; D006025:Glycosaminoglycans / Q000378:metabolism; D006801:Humans; D008288:Malaria / Q000469:parasitology; D008956:Models, Chemical; D008969:Molecular Sequence Data; D010963:Plasmodium falciparum / Q000378:metabolism*; D011247:Pregnancy; D013997:Time Factors
chemical_list: D000953:Antigens, Protozoan; D006025:Glycosaminoglycans; D002809:Chondroitin Sulfates