Published online Nov 7, 2007. doi: 10.3748/wjg.v13.i41.5497
Revised: August 21, 2007
Accepted: September 24, 2007
Published online: November 7, 2007
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 overnight 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 down-regulated 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.