Redox regulation of interleukin-8 expression in MKN28 cells

Dig Dis Sci. 1999 Feb;44(2):266-73. doi: 10.1023/a:1026638014062.


Recent evidence suggests a role of reactive oxygen intermediates (ROI) in intracellular signaling and regulation of gene expression. We examined whether expression of interleukin-8 (IL-8), a key cytokine in the inflammatory responses of gastric epithelial cells, is sensitive to antioxidants and oxidative stress. IL-8 secretion was quantified by IL-8 enzyme-linked immunosorbent assay, and IL-8 mRNA expression was determined by northern blot analysis. Electrophoretic mobility shift assay was performed to detect the transcription factor, nuclear factor kappaB (NF-kappaB). N-Acetylcysteine (NAC) or dimethylsulfoxide inhibited IL-8 expression induced by tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta (IL-1beta). Externally applied H2O2 significantly up-regulated IL-8 expression. TNF-alpha-induced activation of NF-kappaB activity was suppressed by NAC, and H2O2 caused significant activation of NF-kappaB. Since ROI production is increased in the inflamed gastric mucosa, for example, in H. pylori-associated gastritis, the present results suggest that ROI may be an important modulator of IL-8 expression in gastric mucosal cells.

MeSH terms

  • Acetylcysteine / pharmacology
  • Blotting, Northern
  • Dimethyl Sulfoxide / pharmacology
  • Electrophoresis
  • Enzyme-Linked Immunosorbent Assay
  • Gastric Mucosa / metabolism*
  • Humans
  • Hydrogen Peroxide / pharmacology
  • Interleukin-1 / pharmacology
  • Interleukin-8 / biosynthesis*
  • NF-kappa B / pharmacology
  • Oxidation-Reduction
  • RNA, Messenger / analysis
  • Reactive Oxygen Species / metabolism*
  • Transcription Factors / analysis
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / pharmacology


  • Interleukin-1
  • Interleukin-8
  • NF-kappa B
  • RNA, Messenger
  • Reactive Oxygen Species
  • Transcription Factors
  • Tumor Necrosis Factor-alpha
  • Hydrogen Peroxide
  • Acetylcysteine
  • Dimethyl Sulfoxide