Abstract
Cigarette smoke is a major risk factor for lung cancer and respiratory infections. This increased susceptibility may result from cigarette smoke-induced impairment of the immune system. In this study, we evaluated the effect of nicotine on the production of inflammatory mediators by activated macrophages. Pretreatment with nicotine caused a significant inhibition of LPS-induced IL-1, IL-8, and PGE2 expression at the transcriptional level in U937 cells. Nicotine inhibited the activation of a transcription factor, NF-kappaB, which in turn, binds to and mediates transcriptional activation of these genes. These inhibitory effects of nicotine may contribute to cigarette smoke-induced immunosuppression.
Copyright 1998 Academic Press.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cyclooxygenase 2
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Cytokines / genetics*
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Dinoprostone / biosynthesis
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Gene Expression Regulation / drug effects*
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Humans
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Inflammation
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Interleukin-1 / genetics
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Interleukin-8 / genetics
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Isoenzymes / biosynthesis
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Isoenzymes / genetics
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Lipopolysaccharides / antagonists & inhibitors
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Lipopolysaccharides / pharmacology*
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Membrane Proteins
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NF-kappa B / metabolism*
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Nicotine / pharmacology*
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Prostaglandin-Endoperoxide Synthases / biosynthesis
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Prostaglandin-Endoperoxide Synthases / genetics
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Transcription, Genetic / drug effects*
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U937 Cells
Substances
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Cytokines
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Interleukin-1
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Interleukin-8
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Isoenzymes
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Lipopolysaccharides
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Membrane Proteins
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NF-kappa B
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Nicotine
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Cyclooxygenase 2
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PTGS2 protein, human
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Prostaglandin-Endoperoxide Synthases
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Dinoprostone