PT  - JOURNAL ARTICLE
AU  - Moss, S F
AU  - Calam, J
AU  - Agarwal, B
AU  - Wang, S
AU  - Holt, P R
TI  - Induction of gastric epithelial apoptosis by Helicobacter pylori.
AID  - 10.1136/gut.38.4.498
DP  - 1996 Apr 01
TA  - Gut
PG  - 498--501
VI  - 38
IP  - 4
4099  - http://gut.bmj.com/content/38/4/498.short
4100  - http://gut.bmj.com/content/38/4/498.full
SO  - Gut1996 Apr 01; 38
AB  - 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.