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Research Article Free access | 10.1172/JCI116097

Oxygen radical scavengers selectively inhibit interleukin 8 production in human whole blood.

L E DeForge, J C Fantone, J S Kenney, and D G Remick

Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.

Find articles by DeForge, L. in: JCI | PubMed | Google Scholar

Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.

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Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.

Find articles by Kenney, J. in: JCI | PubMed | Google Scholar

Department of Pathology, University of Michigan Medical School, Ann Arbor 48109-0602.

Find articles by Remick, D. in: JCI | PubMed | Google Scholar

Published November 1, 1992 - More info

Published in Volume 90, Issue 5 on November 1, 1992
J Clin Invest. 1992;90(5):2123–2129. https://doi.org/10.1172/JCI116097.
© 1992 The American Society for Clinical Investigation
Published November 1, 1992 - Version history
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Abstract

The hydroxyl radical (OH.) scavenger dimethyl sulfoxide (DMSO) was found to dose-dependently inhibit interleukin 8 (IL-8) production in LPS-stimulated human whole blood. At a concentration of 1% (vol/vol), DMSO blocked IL-8 release by approximately 90% in the presence of 1 microgram/ml LPS at a 24-h time point, but did not affect cell viability or reduce the production of tumor necrosis factor (TNF), interleukin 6, or interleukin-1 beta (IL-1 beta). DMSO was found to directly inhibit IL-8 expression at the level of transcription. Furthermore, this effect was not LPS-specific, in that IL-8 production was reduced by DMSO to a similar extent upon stimulation of blood with phytohemagglutinin, aggregated immune complexes, TNF, or IL-1 beta. Other oxygen radical scavengers that have been shown to inhibit OH.-dependent reactions (dimethyl thiourea, thiourea, mannitol, and ethanol) also inhibited IL-8 production. Conversely, addition of H2O2 caused a dose-dependent stimulation of IL-8 release. These results provide evidence that reactive oxygen metabolites play an important role in the regulation of IL-8 production and suggest that reduction of IL-8 release may contribute to the beneficial effects of antioxidants in experimental models of inflammation and ischemia/reperfusion injury.

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