Induction of human beta-defensin-2 mRNA expression by Helicobacter pylori in human gastric cell line MKN45 cells on cag pathogenicity island

Biochem Biophys Res Commun. 1999 Oct 5;263(3):770-4. doi: 10.1006/bbrc.1999.1452.

Abstract

Helicobacter pylori is an etiological agent of gastritis, peptic ulcer, and gastric cancer. Human beta-defensin-2 (hBD-2) is an antimicrobial peptide which belongs to one of the most important host defense systems against bacterial infection in several epithelial tissues. We studied the effect of H. pylori on the expression of hBD-2 mRNA in MKN45 gastric mucosal cells. H. pylori, but not culture filtrate, increased the hBD-2 mRNA level in MKN45 cells; the inductive effect of H. pylori was not detected with Intestine 407 cells. Among H. pylori strains, strain OHPC0002, which lacks a cag Pathogenicity Island (PAI), did not induce hBD-2 mRNA in MKN45 cells. These results suggested that H. pylori cag PAI is critical for the induction of hBD-2 mRNA in MKN45 cells. Exposure of MKN45 cells to Salmonella typhimurium, S. enteritidis, S. typhi, and S. dublin, but not Escherichia coli ML35, also resulted in induction of hBD-2 mRNA.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blood Bactericidal Activity / genetics
  • Cell Line
  • Defensins
  • Escherichia coli / physiology
  • Gastric Mucosa / metabolism*
  • Gastric Mucosa / microbiology*
  • Gene Expression Regulation*
  • Helicobacter pylori / pathogenicity*
  • Helicobacter pylori / physiology*
  • Humans
  • Intestinal Mucosa
  • Organ Specificity
  • Polymerase Chain Reaction
  • Proteins / genetics*
  • RNA, Messenger / genetics
  • Salmonella / physiology
  • Salmonella enteritidis / physiology
  • Salmonella typhi / physiology
  • Salmonella typhimurium / physiology
  • Species Specificity
  • Transcription, Genetic*

Substances

  • Defensins
  • Proteins
  • RNA, Messenger