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. 1996 Apr;38(4):498–501. doi: 10.1136/gut.38.4.498

Induction of gastric epithelial apoptosis by Helicobacter pylori.

S F Moss 1, J Calam 1, B Agarwal 1, S Wang 1, P R Holt 1
PMCID: PMC1383103  PMID: 8707076

Abstract

BACKGROUND--Helicobacter pylori may promote gastric carcinogenesis through increasing gastric epithelial cell proliferation. How H pylori does so is unknown. Programmed, non-necrotic, cell death (apoptosis) occurs throughout the gut and is linked to proliferation. It was hypothesised that H pylori may induce hyper-proliferation through increasing apoptosis. AIM--To measure the effect of H pylori infection on gastric epithelial apoptosis in situ. PATIENTS--Patients with duodenal ulcers treated to eradicate H pylori and patients with H pylori negative non-ulcer dyspepsia. METHODS--Retrospective quantification of apoptotic epithelial cells in situ from formalin fixed biopsy specimens, counted after staining by terminal uridine deoxynucleotidyl nick end-labelling. RESULTS--In the uninfected stomach, apoptotic cells were rare and situated in the most superficial portion of gastric glands (mean 2.9% of epithelial cells). In H pylori infection, they were more numerous and were located throughout the depth of gastric glands, comprising 16.8% of epithelial cells, falling to 3.1% after H pylori eradication, p = 0.017. Apoptotic cell number did not correlate with the degree of histological gastritis. CONCLUSIONS--These results suggest that H pylori induces epithelial apoptosis in vivo. Increased apoptosis may be the stimulus for a compensatory hyperproliferative and potentially preneoplastic response in chronic H pylori infection.

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Selected References

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