Nicotine inhibits the production of inflammatory mediators in U937 cells through modulation of nuclear factor-kappaB activation

Biochem Biophys Res Commun. 1998 Nov 9;252(1):25-8. doi: 10.1006/bbrc.1998.9599.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cyclooxygenase 2
  • Cytokines / genetics*
  • Dinoprostone / biosynthesis
  • Gene Expression Regulation / drug effects*
  • Humans
  • Inflammation
  • Interleukin-1 / genetics
  • Interleukin-8 / genetics
  • Isoenzymes / biosynthesis
  • Isoenzymes / genetics
  • Lipopolysaccharides / antagonists & inhibitors
  • Lipopolysaccharides / pharmacology*
  • Membrane Proteins
  • NF-kappa B / metabolism*
  • Nicotine / pharmacology*
  • Prostaglandin-Endoperoxide Synthases / biosynthesis
  • Prostaglandin-Endoperoxide Synthases / genetics
  • Transcription, Genetic / drug effects*
  • U937 Cells

Substances

  • Cytokines
  • Interleukin-1
  • Interleukin-8
  • Isoenzymes
  • Lipopolysaccharides
  • Membrane Proteins
  • NF-kappa B
  • Nicotine
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Prostaglandin-Endoperoxide Synthases
  • Dinoprostone