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 alpha 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.