Helicobacter pylori CagA status and colonized gastric mucosa proliferation and apoptosis

H. pylori infection may influence the turnover of gastric epithelial cells. We determined whether the variable cagA status of H. pylori is relevant for proliferation and apoptosis of colonized gastric mucosa cells. Mucosal biopsies from gastric antrum, corpus and fundus of each of 18 H. pylori infected patients with non-ulcer dyspepsia, were cultured onto blood agar. H. pylori colonies – from 5 to 25 colonies per biopsy – were examined for the presence of cagA gene by hybridization. Biopsy sections were stained with haematoxylin/eosin and examined for inflammation, atrophy and intestinal metaplasia. Gastric glandular cell proliferation was assessed by evaluating the expression of PCNA and apoptosis by the TUNEL method. Overall 729 colonies were examined; 329 colonies (45.1%) were cagA+; 400 colonies (54.8%) were cagA-. All colonies from four patients were cagA+, and all colonies from two patients were cagA-. In 11 patients (61.1%) both cagA+ and cagA- colonies were found. High levels of cell proliferation were associated with histological atrophy, but not with the possession of cagA by organisms colonizing the same mucosal sites. Mean apoptotic indexes (SD) of gastric mucosa cells colonized by all cagA-, all cagA+ and cagA mixed organisms were respectively 1.18 (0.53), 1.58 (0.95) and 1.11 (1.05) (p< 0.001). Results of these in ex-vivo tests suggest that the cagA status of infecting organisms may contribute to regulate apoptosis of gastric epithelial cells, while cell proliferation is not influences by the presence of the cagA gene, but by the occurrence of gastric mucosa atrophy.