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

Objective To investigate the mechanisms underlying the hypergastrinaemia of Helicobacter pylori by examining the effects of H. pylori on basal and sti mulated gastrin release from cultured canine G-cells. Methods Canine antral G-cells were prepared by collagenase-EDTA digestion a nd cultured for 40 h, G-cells were then cultured for a further 24 h with tw o different H. pylori sonicates before basal and bombesin-stimulated gastri n release were measured by radioimmunoassay. Results Treatment of G-cells with both H. pylori sonicates significantly en hanced basal gastrin release (by 17-27%) and bombesin-stimulated gastrin re lease (by 115-133%). This effect was independent of cagA and vacuolating cy totoxin status. Control treatment with Escherichia coli sonicate had no eff ect on gastrin release, There was no change in the cellular content of gast rin. Conclusions Incubation of antral G-cells with H. pylori constituents enhanc es 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. (C) 2000 Lippincott William s & Wilkins.