Effect of Helicobacter pylori products and recombinant cytokines on gastrin release from cultured canine G cells

Background & Aims: The pathophysiology of hypergastrinemia in Helicobacter pylori infection is undefined, but the infected antrum shows a marked inflammatory response with local production of cytokines, Hypergastrinemia and inflammatory infiltrate clear with successful eradication, The aim of this study was to examine whether the cytokines tumor necrosis factor a or interleukin 8 (IL-8), which are produced in the gastric mucosa of patients with H. pylori-induced peptic disease or H. pylori products, can stimulate gastrin release from isolated cultured canine G cells. Methods: Canine G cells were isolated by collagenase digestion, enriched by centrifugal elutriation, incubated with cytokines, bacterial components, or both, and gastrin release was measured by radioimmunoassay, Results: IL-8 (1 and 10 nmol/L) stimulated gastrin release by 34% +/- 13% and 43% +/- 23% (P < 0.05) above basal, respectively, H. pylori sonicates, water extract preparations, and lipopolysaccharide had no stimulatory actions, but the sonicates from two of four strains potentiated the effects of IL-8, leading to maximal gastrin release of 230% +/- 130% and 232% +/- 33% above basal, respectively (P < 0.05), Conclusions: IL-8 stimulated gastrin release from isolated G cells, and the effect was potentiated by H, pylori products, The interaction of cytokines and H. pylori may contribute to the hypergastrinemia seen in vivo.