Abstract
Supplementation with vitamin A potentiates host resistance to malaria, however, the underlying mechanism is unknown. We tested the effects of 9-cis-retinoic acid, a metabolite of vitamin A, on CD36 expression, non-opsonic phagocytic clearance of parasitised erythrocytes, and TNFalpha production in human monocytes and macrophages. We found reduced secretion of TNFalpha, upregulated CD36 expression, and increased phagocytosis of Plasmodium falciparum-parasitised erythrocytes. Increased parasite clearance and reduced proinflammatory cytokine responses to infection might partly explain the beneficial effects of supplementation with vitamin A in malaria.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alitretinoin
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Animals
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Antiprotozoal Agents / administration & dosage
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Antiprotozoal Agents / pharmacology*
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CD36 Antigens / drug effects
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Child
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Erythrocytes / drug effects
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Erythrocytes / metabolism
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Erythrocytes / parasitology
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Humans
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Malaria, Falciparum / blood*
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Malaria, Falciparum / drug therapy*
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Phagocytosis / drug effects
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Plasmodium falciparum / drug effects*
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Tretinoin / administration & dosage
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Tretinoin / pharmacology*
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Tumor Necrosis Factor-alpha / metabolism
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Up-Regulation / drug effects
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Vitamin A / administration & dosage
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Vitamin A / pharmacology*
Substances
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Antiprotozoal Agents
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CD36 Antigens
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Tumor Necrosis Factor-alpha
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Vitamin A
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Alitretinoin
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Tretinoin