Helicobacter pylori infection triggers aberrant expression of activation-induced cytidine deaminase in gastric epithelium

Nat Med. 2007 Apr;13(4):470-6. doi: 10.1038/nm1566. Epub 2007 Apr 1.


Infection with Helicobacter pylori (H. pylori) is a risk factor for the development of gastric cancer. Here we show that infection of gastric epithelial cells with 'cag' pathogenicity island (cagPAI)-positive H. pylori induced aberrant expression of activation-induced cytidine deaminase (AID), a member of the cytidine-deaminase family that acts as a DNA- and RNA-editing enzyme, via the IkappaB kinase-dependent nuclear factor-kappaB activation pathway. H. pylori-mediated upregulation of AID resulted in the accumulation of nucleotide alterations in the TP53 tumor suppressor gene in gastric cells in vitro. Our findings provide evidence that aberrant AID expression caused by H. pylori infection might be a mechanism of mutation accumulation in the gastric mucosa during H. pylori-associated gastric carcinogenesis.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, Bacterial / metabolism
  • Bacterial Proteins / metabolism
  • Cytidine Deaminase / metabolism*
  • DNA Primers
  • Gastric Mucosa / metabolism*
  • Gene Expression Regulation, Neoplastic*
  • Genes, p53 / genetics*
  • Helicobacter Infections / genetics*
  • Helicobacter Infections / metabolism
  • Humans
  • Immunohistochemistry
  • Models, Biological
  • Mutagenesis / genetics
  • NF-kappa B / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction / physiology
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / microbiology


  • Antigens, Bacterial
  • Bacterial Proteins
  • DNA Primers
  • NF-kappa B
  • cagA protein, Helicobacter pylori
  • AICDA (activation-induced cytidine deaminase)
  • Cytidine Deaminase