Helicobacter pylori increases gastrin release from cultured canine antral G-cells.

Abstract

To investigate the mechanisms underlying the hypergastrinaemia of Helicobacter pylori by examining the effects of H. pylori on basal and stimulated gastrin release from cultured canine G-cells. Canine antral G-cells were prepared by collagenase-EDTA digestion and cultured for 40 h. G-cells were then cultured for a further 24 h with two different H. pylori sonicates before basal and bombesin-stimulated gastrin release were measured by radioimmunoassay. Treatment of G-cells with both H. pylori sonicates significantly enhanced basal gastrin release (by 17-27%) and bombesin-stimulated gastrin release (by 115-133%). This effect was independent of cagA and vacuolating cytotoxin status. Control treatment with Escherichia coli sonicate had no effect on gastrin release. There was no change in the cellular content of gastrin. Incubation of antral G-cells with H. pylori constituents enhances subsequent basal and bombesin-stimulated gastrin release. Direct contact between H. pylori and G-cells in the gastric antrum may be responsible for the hypergastrinaemia seen with the infection.