Abstract
Although dietary fatty acids can modulate atherogenesis and inflammation, the mechanisms by which this occurs are poorly understood. Induction in endothelial cells of adhesion molecules for circulating leukocytes and of inflammatory mediators by cytokines likely contributes to early phases of atherogenesis and inflammation. We report here that incorporation into cellular lipids of one specific fatty acid of the omega-3 family, docosahexaenoic acid (DHA), decreases cytokine-induced expression of endothelial leukocyte adhesion molecules, secretion of inflammatory mediators, and leukocyte adhesion to endothelial cells. These properties of DHA may contribute to antiatherogenic and antiinflammatory effects of omega-3 fatty acids.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adult
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Cell Adhesion Molecules / metabolism*
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Cells, Cultured
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Docosahexaenoic Acids / pharmacology*
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Dose-Response Relationship, Drug
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E-Selectin
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Endothelium, Vascular / cytology
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Endothelium, Vascular / metabolism
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Fatty Acids, Omega-3 / pharmacology*
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Humans
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Inflammation Mediators / metabolism*
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Intercellular Adhesion Molecule-1 / metabolism
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Interleukin-1 / pharmacology
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Interleukin-4 / pharmacology
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Interleukin-6
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Interleukin-8
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Tumor Necrosis Factor-alpha / pharmacology
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Vascular Cell Adhesion Molecule-1
Substances
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Cell Adhesion Molecules
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E-Selectin
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Fatty Acids, Omega-3
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Inflammation Mediators
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Interleukin-1
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Interleukin-6
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Interleukin-8
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Tumor Necrosis Factor-alpha
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Vascular Cell Adhesion Molecule-1
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Intercellular Adhesion Molecule-1
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Interleukin-4
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Docosahexaenoic Acids