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Effects of Helicobacter pylori on the cadherin–catenin complex

¹ Wolfson Centre for Digestive Diseases and Institute of Infections, Inflammation and Immunity, University Hospital Nottingham, Nottingham, UK
² Centre for Integrated Systems Biology and Medicine, School of Biomedical Sciences, University Hospital Nottingham
³ Department of Histopathology, University Hospital Nottingham

Correspondence to:
J R Bebb
Wolfson Centre for Digestive Diseases, University Hospital, Nottingham, NG7 2UH; jamesbebb{at}doctors.org.uk Background: The cadherin–catenin complex is the key component of the adherens junction in epithelial cells, and changes in this complex are implicated in gastric adenocarcinoma. Germline mutations in E-cadherin have been described in diffuse-type gastric adenocarcinoma. Helicobacter pylori infection is the first stage in gastric carcinogenesis.

Aims: To determine whether H pylori was associated with changes in the complex, and whether this was affected by virulence of the strain.

Methods: Epithelial cell lines were cultured with H pylori using the wild-type pathogenic and non-pathogenic strains and CagE null and VacA null isogenic mutants. Gastric biopsy specimens at endoscopy were obtained from patients with (n = 17) and without (n = 15) H pylori infection, and E-cadherin and ß–catenin expression was assessed by immunohistochemistry. H pylori was typed by polymerase chain reaction from these patients for CagE and VacA.

Results: In vitro studies showed that coculture with a pathogenic strain of H pylori led to disruption of epithelial junctional ß-catenin expression, but without evidence of nuclear translocation or signalling. This effect was independent of a functional Cag pathogenicity island and vacuolating activity, but dependent on live bacteria. No marked differences in ß-catenin or E-cadherin expression were seen in gastric biopsy specimens in patients with and without H pylori infection.

Conclusion: Acute H pylori infection disrupts junctional ß-catenin in vitro, but chronic infection by H pylori has no effect on E-cadherin and ß-catenin expression, as seen in gastric biopsy specimens at the initial gastritis stage of the proposed Correa pathway of gastric carcinogenesis. A later effect at the later stages of atrophy or intestinal metaplasia cannot be ruled out.