Interleukin-8 Production by Macrophages From Atheromatous Plaques
Interleukin-8 (IL-8) is a chemotactic peptide produced by macrophages that may be involved in the recruitment of inflammatory cells into atherosclerotic plaques. In vitro, IL-8 production by macrophages isolated from carotid plaques (1240 plus/minus 510 pg. 10 cells sup -1 *symbol* 24 h sup -1, mean...
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Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 1996-08, Vol.16 (8), p.1007-1012 |
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Sprache: | eng |
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Zusammenfassung: | Interleukin-8 (IL-8) is a chemotactic peptide produced by macrophages that may be involved in the recruitment of inflammatory cells into atherosclerotic plaques. In vitro, IL-8 production by macrophages isolated from carotid plaques (1240 plus/minus 510 pg. 10 cells sup -1 *symbol* 24 h sup -1, mean plus/minus SEM, n = 6) and noncarotid plaques (4312 plus/minus 1588 pg *symbol* 10 cells sup -1 24 h sup -1, n = 9) was significantly greater than IL-8 production by blood monocytes isolated from the same patients (526 plus/minus 278 pg. 10 cells sup -1 24 h sup -1, n = 6, P < .05 and 726 plus/minus 384 pg *symbol* 10 cells sup -1 *symbol* 24 h sup -1, n = 9, P < .01, respectively). IL-8 produced by atherosclerotic macrophages was demonstrated to be biologically active in a neutrophil chemotaxis assay. IL-8 mRNA was detectable in plaque macrophages and blood monocytes from these patients, but blood monocytes from normal donors did not exhibit detectable IL-8 mRNA. IL-8 mRNA was localized in macrophage-rich areas of atherosclerotic plaques by in situ hybridization. These studies demonstrate that macrophages from atherosclerotic plaques show an enhanced capacity to produce IL-8 compared with normal and patient blood monocytes and that macrophages are a major site of IL-8 mRNA production in atherosclerotic plaques. These results provide further evidence for a proinflammatory role for macrophages in atherosclerosis. (Arterioscler Thromb Vasc Biol. 1996;16:1007-1012.) |
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ISSN: | 1079-5642 1524-4636 |
DOI: | 10.1161/01.atv.16.8.1007 |