Helicobacter pylori-mediated transcriptional regulation of the human beta-defensin 2 gene requires NF-kappaB

Cell Microbiol. 2001 Feb;3(2):115-23. doi: 10.1046/j.1462-5822.2001.00096.x.


Human beta-defensin 2 (hBD-2) is an antimicrobial peptide involved in host defence against bacterial infection in epithelial tissues. Its levels are dramatically increased after bacterial infection. The involvement of NF-kappaB in Helicobacter pylori-mediated induction of hBD-2 promoter activity was examined. A luciferase reporter plasmid containing the hBD-2 promoter extending from -2110 base pairs to -1 was transiently expressed in MKN45 cells, and promoter activity was determined after incubation with H. pylori for 6 h. Deletion or mutation of the NF-kappaB site at -208 abolished activation of the hBD-2 promoter. Only H. pylori strains carrying a cag pathogenicity island (PAI) induced activation of the NF-kappaB site of the hBD-2 promoter gene. By gel retardation analyses, H. pylori increased NF-kappaB binding to hBD-2 promoter gene sequences. Supershift analysis demonstrated that whereas H. pylori activated NF-kappaB p65-p65 and p50-p50 homodimers, and the p65-p50 heterodimer of NF-kappaB, only the p65-p65 homodimer bound to the NF-kappaB site of the hBD-2 promoter. Thus, specific NF-kappaB proteins are important cis-elements for induction of hBD-2 gene transcription by H. pylori.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line
  • Gastric Mucosa / microbiology*
  • Gene Expression Regulation
  • Helicobacter pylori / pathogenicity*
  • Humans
  • NF-kappa B / metabolism*
  • Promoter Regions, Genetic
  • Transcription, Genetic
  • beta-Defensins / genetics*


  • DEFB4A protein, human
  • NF-kappa B
  • beta-Defensins