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AIM: To explore the effects of H pylori infection on gap-junctional intercellular communication (GJIC) and proliferation of gastric epithelial cells in vitro. METHODS: A human gastric epithelial cell line (SGC-7901) cultured on coverslips was exposed ovight to intact H pylori (CagA+ or CagA- strains) and sonicated extracts, respectively. GJIC between the cells was detected by fluorescence redistribution after photobleaching (FRAP) technique. Proliferation of SGC cells was determined by methylthiazolyl tetrazolium (MTT)assay.RESULTS: When compared with control in which cells were cultured with simple medium alone, both CagA+ and CagA- H pylori isolates could inhibit GJIC (CagA+:F = 57.98, P ＜ 0.01; CagA-: F = 29.59, P ＜ 0.01) and proliferation (CagA+: F = 42.65, P ＜ 0.01; CagA-: F =58.14, P ＜ 0.01) of SGC-7901 cells. Compared with CagA- strains, CagA+ H pylori more significantly downregulated GJIC of gastric cells (intact H pylori: t = 13.86,P ＜ 0.01; sonicated extracts: t = 11.87, P ＜ 0.01) and inhibited proliferation gastric cells to a lesser extent in vitro (intact H pylori: t = 3.06, P ＜ 0.05; sonicated extracts: t = 3.94, P ＜ 0.01).CONCLUSION: Compared with CagA- H pylori strains,CagA+ strains down-regulate GJIC of gastric epithelial cells more significantly and inhibit proliferation of gastric cells to a lesser extent in vitro. H pylori, especially CagA+ strains, may play an important role in gastric carcinogenesis.