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

I. Beales, Martin Blaser, S. Srinivasan, J. Calam, G. I. Perez-Perez, T. Yamada, J. Scheiman, L. Post, J. Del Valle

Research output: Contribution to journalArticlepeer-review

91 Scopus citations


Background and 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 α 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% ± 1.3% 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.

Original languageEnglish (US)
Pages (from-to)465-471
Number of pages7
Issue number2
StatePublished - Jan 1 1997
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Hepatology
  • Gastroenterology

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