Effects of Helicobacter pylori on the cadherin-catenin complex
| Autor: | Lopa Leach, James R. Bebb, Neil Hand, Darren P. Letley, Rachael J. Thomas, John Atherton, Abed M. Zaitoun |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Pathology
medicine.medical_specialty Biopsy Spirillaceae Blotting Western Cell Line Helicobacter Infections Pathology and Forensic Medicine medicine Gastric mucosa Humans Helicobacter pylori Virulence biology medicine.diagnostic_test Cadherin Intestinal metaplasia Catenins Epithelial Cells General Medicine Cadherins medicine.disease biology.organism_classification Molecular biology Coculture Techniques medicine.anatomical_structure Gastric Mucosa Gastritis Original Article Catenin complex medicine.symptom |
| Zdroj: | Journal of Clinical Pathology. 59:1261-1266 |
| ISSN: | 0021-9746 |
| Popis: | 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 β–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 β-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 β-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 β-catenin in vitro, but chronic infection by H pylori has no effect on E-cadherin and β-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. |
| Databáze: | OpenAIRE |
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