Thrombospondin Mediates the Cytoadherence of Plasmodium falciparum-Infected Red Cells to Vascular Endothelium in Shear Flow Conditions

Cerebral malaria is thought to involve specific attachment of Plasmodium falciparum-infected knobby red cells to venular endothelium. The nature of surface ligands on host endothelial cells that may mediate cytoadherence is poorly understood. We have investigated the effects of soluble thrombospondi...

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Bibliographic Details
Published in:Blood 1988-01, Vol.71 (1), p.71-75
Main Authors: Rock, Edwin P., Roth jr, Eugene F., Rojas-Corona, Rogelio R., Sherwood, James A., Nagel, Ronald L., Howard, Russell J., Kaul, Dhananjaya K.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cell Adhesion - drug effects
Endothelium, Vascular - physiology
Erythrocytes - drug effects
Erythrocytes - parasitology
Fibrinogen - pharmacology
Fibronectins - pharmacology
Fundamental and applied biological sciences. Psychology
Glycoproteins - pharmacology
Human protozoal diseases
Infectious diseases
Life cycle. Host-agent relationship. Pathogenesis
Malaria
Malaria - blood
Medical sciences
Parasitic diseases
Plasmodium falciparum
Protozoa
Protozoal diseases
Rats
Stress, Mechanical
Thrombospondins
Tropical medicine
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Summary:Cerebral malaria is thought to involve specific attachment of Plasmodium falciparum-infected knobby red cells to venular endothelium. The nature of surface ligands on host endothelial cells that may mediate cytoadherence is poorly understood. We have investigated the effects of soluble thrombospondin, rabbit antiserum raised against throm-bospondin, and human immune serum on cytoadherence of parasitized erythrocytes in ex vivo mesocecum vasculature. Preincubation of infected red cells with soluble thrombospondin or human immune serum inhibits binding of infected red cells to rat venular endothelium. Infusion of the microcirculatory preparation with rabbit antithrombo-spondin antibodies before perfusion of parasitized erythrocytes also resulted in decreased cytoadherence. In addition, incubation of infected cells with human immune sera obtained from malaria patients significantly inhibited the observed cytoadherence. Our results indicate that throm-bospondin mediates binding of infected red cells to venular endothelium and may thus be involved in the pathogenesis of cerebral malaria.
ISSN:0006-4971
1528-0020
DOI:10.1182/blood.V71.1.71.71