Abstract
In this review the old concept of severe malaria as a toxic disease is re-examined in the light of recent discoveries in the field of cytokines. Animal studies suggest that the induction of TNF by parasite-derived molecules may be partly responsible for cerebral malaria and anemia, while hypoglycaemia may be due to direct effects of similar molecules on glucose metabolism. These molecules appear to be phospholipids and we suggest that when fully characterized they might form the basis of antitoxic therapy for malaria.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Anemia / etiology
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Animals
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Antigens, Protozoan / immunology*
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Cytokines / antagonists & inhibitors
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Cytokines / biosynthesis*
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Humans
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Hypoglycemia / etiology
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Macrophages / metabolism
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Malaria, Cerebral / etiology*
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Malaria, Cerebral / prevention & control
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Mice
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Mice, Inbred C57BL
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Mice, Inbred CBA
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Phospholipids / immunology
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Plasmodium / immunology*
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Toxins, Biological / immunology*
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Tumor Necrosis Factor-alpha / antagonists & inhibitors
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Tumor Necrosis Factor-alpha / biosynthesis
Substances
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Antigens, Protozoan
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Cytokines
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Phospholipids
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Toxins, Biological
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Tumor Necrosis Factor-alpha