Helicobacter pylori infection activates NF-kappa B in gastric epithelial cells

Gastroenterology. 1997 Oct;113(4):1099-109. doi: 10.1053/gast.1997.v113.pm9322504.


Background & aims: Helicobacter pylori adheres to gastric epithelial cells and stimulates interleukin (IL)-8 production. This may be instrumental in neutrophil infiltration of the gastric epithelium that characterizes H. pylori gastritis. This study examined the molecular mechanisms leading to H. pylori-induced epithelial cell IL-8 production.

Methods: Electrophoretic mobility shift analyses for NF-kappa B were performed on cell and nuclear extracts from H. pylori-infected AGS and Kato III human gastric epithelial cells.

Results: H. pylori infection activated the transcription factor NF-kappa B and induced nuclear translocation of both NF-kappa B p50/p65 heterodimers and p50 homodimers. Nuclear translocation of NF-kappa B (30 minutes) was followed by increased IL-8 messenger RNA (1 hour) and protein levels (4 hours) consistent with NF-kappa B up-regulation of IL-8 gene transcription. Pretreatment of AGS cells with PDTC, which blocks NF-kappa B activation, inhibited H. pylori-induced increases in IL-8 production by 90%. Immunohistochemical studies using a monoclonal antibody that recognizes the I-kappa B binding region of p65 showed activated NF-kappa B in gastric epithelial cells of patients with H. pylori gastritis.

Conclusions: H. pylori infection activates NF-kappa B in gastric epithelial cells in vitro and in vivo. NF-kappa B is a transcriptional regulator of IL-8 production, and its activation after bacterial infection may be an important defense response in gastrointestinal epithelial cells.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Biopsy
  • Cell Line
  • Cell Nucleus / metabolism
  • Gastric Mucosa / microbiology*
  • Gastric Mucosa / pathology
  • Gastric Mucosa / physiology*
  • Genes, MHC Class I
  • Helicobacter Infections / pathology
  • Helicobacter Infections / physiopathology*
  • Helicobacter pylori / pathogenicity
  • Helicobacter pylori / physiology*
  • Humans
  • Interleukin-1 / pharmacology
  • Interleukin-8 / biosynthesis*
  • NF-kappa B / biosynthesis
  • NF-kappa B / isolation & purification
  • NF-kappa B / metabolism*
  • RNA, Messenger / biosynthesis
  • Recombinant Proteins / pharmacology
  • Transcription, Genetic* / drug effects


  • Interleukin-1
  • Interleukin-8
  • NF-kappa B
  • RNA, Messenger
  • Recombinant Proteins