Document Detail


Complement receptor 1 is a sialic acid-independent erythrocyte receptor of Plasmodium falciparum.
MedLine Citation:
PMID:  20585558     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Plasmodium falciparum is a highly lethal malaria parasite of humans. A major portion of its life cycle is dedicated to invading and multiplying inside erythrocytes. The molecular mechanisms of erythrocyte invasion are incompletely understood. P. falciparum depends heavily on sialic acid present on glycophorins to invade erythrocytes. However, a significant proportion of laboratory and field isolates are also able to invade erythrocytes in a sialic acid-independent manner. The identity of the erythrocyte sialic acid-independent receptor has been a mystery for decades. We report here that the complement receptor 1 (CR1) is a sialic acid-independent receptor for the invasion of erythrocytes by P. falciparum. We show that soluble CR1 (sCR1) as well as polyclonal and monoclonal antibodies against CR1 inhibit sialic acid-independent invasion in a variety of laboratory strains and wild isolates, and that merozoites interact directly with CR1 on the erythrocyte surface and with sCR1-coated microspheres. Also, the invasion of neuraminidase-treated erythrocytes correlates with the level of CR1 expression. Finally, both sialic acid-independent and dependent strains invade CR1 transgenic mouse erythrocytes preferentially over wild-type erythrocytes but invasion by the latter is more sensitive to neuraminidase. These results suggest that both sialic acid-dependent and independent strains interact with CR1 in the normal red cell during the invasion process. However, only sialic acid-independent strains can do so without the presence of glycophorin sialic acid. Our results close a longstanding and important gap in the understanding of the mechanism of erythrocyte invasion by P. falciparum that will eventually make possible the development of an effective blood stage vaccine.
Authors:
Carmenza Spadafora; Gordon A Awandare; Karen M Kopydlowski; Jozsef Czege; J Kathleen Moch; Robert W Finberg; George C Tsokos; José A Stoute
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-06-17
Journal Detail:
Title:  PLoS pathogens     Volume:  6     ISSN:  1553-7374     ISO Abbreviation:  PLoS Pathog.     Publication Date:  2010  
Date Detail:
Created Date:  2010-06-29     Completed Date:  2010-10-27     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101238921     Medline TA:  PLoS Pathog     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e1000968     Citation Subset:  IM    
Affiliation:
Department of Medicine, the Uniformed Services University of the Health Sciences, Bethesda, Maryland, United States of America.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Western
Erythrocytes / metabolism*,  parasitology*
Flow Cytometry
Fluorescent Antibody Technique
Humans
Immunoprecipitation
Malaria, Falciparum / metabolism*,  virology
Membrane Glycoproteins / metabolism*
Merozoites / physiology
Mice
Mice, Inbred C57BL
Mice, Transgenic
N-Acetylneuraminic Acid / metabolism*
Plasmodium falciparum / physiology*
Receptors, Complement / metabolism*
Receptors, Immunologic / metabolism*
Grant Support
ID/Acronym/Agency:
D43 TW06239/TW/FIC NIH HHS; HL 71502/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Membrane Glycoproteins; 0/Receptors, Complement; 0/Receptors, Immunologic; 0/erythrocyte receptor; 131-48-6/N-Acetylneuraminic Acid
Comments/Corrections

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