Air pollution particles induce IL-6 gene expression in human airway epithelial cells via NF-kappaB activation

Am J Respir Cell Mol Biol. 1998 Jul;19(1):98-106. doi: 10.1165/ajrcmb.19.1.3132.


Fine particles in the air have been associated with increased mortality and morbidity. Particulate air pollution is a complex mixture which varies by region and includes a number of components including residual oil fly ash (ROFA), a byproduct of power plant and industry fuel-oil combustion. Human airway epithelial cells exposed to ROFA release inflammatory cytokines including interleukin (IL)-6, IL-8, and tumor necrosis factor. Expression of these genes is dependent upon pretranscriptional binding of cis regulatory elements, including nuclear factor kappaB (NF-kappaB). To investigate the role of NF-kappaB in the particulate-induced IL-6 response, we exposed human airway epithelial cells (BEAS-2B) to ROFA in vitro. ROFA stimulated a time- and dose-dependent increase in IL-6 messenger RNA (mRNA), which was preceded by the activation of nuclear proteins binding to the NF-kappaB sequence motif in the IL-6 promoter. Transient transfection of BEAS-2B cells with the 5' promoter region of the IL-6 gene linked to a luciferase reporter gene confirmed that NF-kappaB binding is necessary for the transcription of IL-6 mRNA. The IL-6 response was inhibited by the metal chelator deferoxamine and the free radical scavenger N-acetyl-L-cysteine, suggesting that the activation of NF-kappaB may be mediated through reactive oxygen intermediates generated by transition metals found in ROFA. Activation of NF-kappaB may therefore be a critical first step in the inflammatory cascade following exposure to particles generated by oil combustion.

MeSH terms

  • Acetylcysteine / pharmacology
  • Air Pollutants / toxicity*
  • Bronchi / cytology
  • Bronchi / drug effects
  • Bronchi / metabolism*
  • Carbon / toxicity
  • Cell Line
  • Coal Ash
  • DNA / metabolism
  • Deferoxamine / pharmacology
  • Epithelial Cells / cytology
  • Epithelial Cells / drug effects
  • Free Radical Scavengers / pharmacology
  • Fuel Oils
  • Gene Expression Regulation*
  • Humans
  • Interleukin-6 / genetics*
  • Metals / toxicity*
  • NF-kappa B / metabolism*
  • Particulate Matter
  • Promoter Regions, Genetic
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Transfection


  • Air Pollutants
  • Coal Ash
  • Free Radical Scavengers
  • Fuel Oils
  • Interleukin-6
  • Metals
  • NF-kappa B
  • Particulate Matter
  • RNA, Messenger
  • Carbon
  • DNA
  • Deferoxamine
  • Acetylcysteine