Effects of H pylori infection on gap-junctional intercellular communication and proliferation of gastric epithelial cells in vitro.

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.