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The effects of cure of Helicobacter pylori infection on the signal transduction of gastric epithelial cells
Author(s) -
Azuma T.,
Yamazaki S.,
Yamakawa A.,
Ito Y.,
Ohtani M.,
Dojo M.,
Yamazaki Y.,
Higashi H.,
Hatakeyama M.
Publication year - 2003
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.18.s1.2.x
Subject(s) - caga , helicobacter pylori , tyrosine phosphorylation , protein tyrosine phosphatase , gastric mucosa , signal transduction , biology , tyrosine , atrophic gastritis , phosphorylation , immunoprecipitation , gastritis , medicine , immunology , cancer research , antibody , stomach , microbiology and biotechnology , biochemistry , gene , virulence
Summary Background : The CagA protein of Helicobacter pylori is directly injected from the bacteria into cells via the bacterial type IV secretion system and undergoes tyrosine phosphorylation in the gastric epithelial cells. Translocated CagA forms a physical complex with the SRC homology 2 domain (SH2)‐containing tyrosine phosphatase SHP‐2, which plays an important role in mitogenic signal transduction in the host cells. Aim : We examined the effect of eradication therapy on the signal transduction pathway of gastric epithelial cells induced by the CagA protein of H. pylori . Methods : Gastric biopsy samples were obtained from 20 H. pylori ‐positive atrophic gastritis patients before, and 3 months after, H. pylori infection eradication therapy, and subjected to immunoblot analysis to detect tyrosine phosphorylated CagA protein and CagA co‐immunoprecipitated endogenous SHP‐2. Results : Tyrosine phosphorylated CagA protein and CagA co‐immunoprecipitated endogenous SHP‐2 were detected in the gastric mucosa from H. pylori ‐positive atrophic gastritis patients. All H. pylori strains from these patients were cagA ‐positive type I strains. After curing H. pylori infection, the tyrosine phosphorylated CagA protein and CagA co‐immunoprecipitated endogenous SHP‐2 disappeared from the gastric mucosa. Conclusion : The cure of infection reduces the stimulated signal transduction of gastric epithelial cells by the translocated CagA protein of H. pylori , and may confer a beneficial effect on the reduction of cancer risk.