SEARCH:   Advanced

Prepublished online as a Blood First Edition Paper on November 14, 2002; DOI 10.1182/blood-2002-07-2016. This Article Full Text Full Text (PDF) Erratum (v104,p3910) All Versions of this Article: 2002-07-2016v1 101/6/2405    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Vogt, A. M. Articles by Wahlgren, M. Search for Related Content PubMed PubMed Citation Articles by Vogt, A. M. Articles by Wahlgren, M. Related Collections Red Cells Cell Adhesion and Motility Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 March 2003, Vol. 101, No. 6, pp. 2405-2411 RED CELLS Heparan sulfate on endothelial cells mediates the binding of Plasmodium falciparum-infected erythrocytes via the DBL1 domain of PfEMP1 Anna M. Vogt, Antonio Barragan, Qijun Chen, Fred Kironde, Dorothe Spillmann, and Mats Wahlgren From the Microbiology and Tumor Biology Center (MTC), Karolinska Institutet, Stockholm, Sweden; the Swedish Institute for Infectious Disease Control (SMI), Stockholm, Sweden; the Department of Biochemistry, University of Makerere, Kampala, Uganda; and the Department of Medical Biochemistry and Microbiology, Biomedical Center, Uppsala University, Uppsala, Sweden. Plasmodium falciparum may cause severe forms of malaria when excessive sequestration of infected and uninfected erythrocytes occurs in vital organs. The capacity of wild-type isolates of P falciparum-infected erythrocytes (parasitized red blood cells [pRBCs]) to bind glycosaminoglycans (GAGs) such as heparin has been identified as a marker for severe disease. Here we report that pRBCs of the parasite FCR3S1.2 and wild-type clinical isolates from Uganda adhere to heparan sulfate (HS) on endothelial cells. Binding to human umbilical vein endothelial cells (HUVECs) and to human lung endothelial cells (HLECs) was found to be inhibited by HS/heparin or enzymes that remove HS from cell surfaces. 35S-labeled HS extracted from HUVECs bound directly to the pRBCs' membrane. Using recombinant proteins corresponding to the different domains of P falciparum erythrocyte membrane protein 1 (PfEMP1), we identified Duffy-binding-like domain-1 (DBL1) as the ligand for HS. DBL1 bound in an HS-dependent way to endothelial cells and blocked the adherence of pRBCs in a dose-dependent manner. 35S-labeled HS bound to DBL1-columns and eluted as a distinct peak at 0.4 mM NaCl. 35S-labeled chondroitin sulfate (CS) of HUVECs did not bind to PfEMP1 or to the pRBCs' membrane. Adhesion of pRBCs of FCR3S1.2 to platelet endothelial cell adhesion molecule-1 (PECAM-1)/CD31, mediated by the cysteine-rich interdomain region 1 (CIDR1), was found be operative with, but independent of, the binding to HS. HS and the previously identified HS-like GAG on uninfected erythrocytes may act as coreceptors in endothelial and erythrocyte binding of rosetting parasites, causing excessive sequestration of both pRBCs and RBCs. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Normark, D. Nilsson, U. Ribacke, G. Winter, K. Moll, C. E. Wheelock, J. Bayarugaba, F. Kironde, T. G. Egwang, Q. Chen, et al. PfEMP1-DBL1{alpha} amino acid motifs in severe disease states of Plasmodium falciparum malaria PNAS, October 2, 2007; 104(40): 15835 - 15840. [Abstract] [Full Text] [PDF] A. Luginbuhl, M. Nikolic, H. P. Beck, M. Wahlgren, and H. U. Lutz Complement Factor D, Albumin, and Immunoglobulin G Anti-Band 3 Protein Antibodies Mimic Serum in Promoting Rosetting of Malaria-Infected Red Blood Cells Infect. Immun., April 1, 2007; 75(4): 1771 - 1777. [Abstract] [Full Text] [PDF] K. Moll, F. Pettersson, A. M. Vogt, C. Jonsson, N. Rasti, S. Ahuja, M. Spangberg, O. Mercereau-Puijalon, D. E. Arnot, M. Wahlgren, et al. Generation of Cross-Protective Antibodies against Plasmodium falciparum Sequestration by Immunization with an Erythrocyte Membrane Protein 1-Duffy Binding-Like 1{alpha} Domain Infect. Immun., January 1, 2007; 75(1): 211 - 219. [Abstract] [Full Text] [PDF] F. Pettersson, A. M. Vogt, C. Jonsson, B. W. Mok, A. Shamaei-Tousi, S. Bergstrom, Q. Chen, and M. Wahlgren Whole-Body Imaging of Sequestration of Plasmodium falciparum in the Rat Infect. Immun., November 1, 2005; 73(11): 7736 - 7746. [Abstract] [Full Text] [PDF] A. Mayor, N. Bir, R. Sawhney, S. Singh, P. Pattnaik, S. K. Singh, A. Sharma, and C. E. Chitnis Receptor-binding residues lie in central regions of Duffy-binding-like domains involved in red cell invasion and cytoadherence by malaria parasites Blood, March 15, 2005; 105(6): 2557 - 2563. [Abstract] [Full Text] [PDF] M. U. Ferreira, M. da Silva Nunes, and G. Wunderlich Antigenic Diversity and Immune Evasion by Malaria Parasites Clin. Vaccine Immunol., November 1, 2004; 11(6): 987 - 995. [Full Text] [PDF] M. S. ABDEL-LATIF, G. CABRERA, C. KOHLER, P. G. KREMSNER, and A. J. F. LUTY ANTIBODIES TO RIFIN: A COMPONENT OF NATURALLY ACQUIRED RESPONSES TO PLASMODIUM FALCIPARUM VARIANT SURFACE ANTIGENS ON INFECTED ERYTHROCYTES Am J Trop Med Hyg, August 1, 2004; 71(2): 179 - 186. [Abstract] [Full Text] [PDF] S. S. Struik, F. M. Omer, K. Artavanis-Tsakonas, and E. M. Riley Uninfected erythrocytes inhibit Plasmodium falciparum-induced cellular immune responses in whole-blood assays Blood, April 15, 2004; 103(8): 3084 - 3092. [Abstract] [Full Text] [PDF] S. Bork, N. Yokoyama, Y. Ikehara, S. Kumar, C. Sugimoto, and I. Igarashi Growth-Inhibitory Effect of Heparin on Babesia Parasites Antimicrob. Agents Chemother., January 1, 2004; 48(1): 236 - 241. [Abstract] [Full Text] [PDF]

	Copyright © 2003 by American Society of Hematology         Online ISSN: 1528-0020