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

2007; Nature Portfolio; Volume: 13; Issue: 4 Linguagem: Inglês

10.1038/nm1566

1546-170X

Yuko Matsumoto, Hiroyuki Marusawa, Kazuo Kinoshita, Yoko Endo, Tadayuki Kou, Toshiyuki Morisawa, Takeshi Azuma, Il‐mi Okazaki, Tasuku Honjo, Tsutomu Chiba,

Immune Cell Function and Interaction

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 IκB kinase–dependent nuclear factor-κB 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.