Tumour necrosis factor alpha stimulates gastrin release from canine and human antral G cells: possible mechanism of the Helicobacter pylori-gastrin link

Eur J Clin Invest. 1996 Jul;26(7):609-11. doi: 10.1046/j.1365-2362.1996.2040517.x.


There is evidence that gastric Helicobacter pylori (Hp) infection promotes duodenal ulceration by releasing gastrin. We therefore asked how Hp releases gastrin. Tumour necrosis factor alpha (TNF-alpha) is up-regulated in Hp gastritis and stimulates hormone release from pituitary cells, so we tested its effect on primary cultures of canine antral G cells and human antral fragments. TNF-alpha pretreatment (100 ng mL-1) of canine G cells significantly increased both basal (by 89%: P < 0.01) and bombesin-stimulated (by 39% P < 0.05) gastrin release. A similar pattern of increase was seen following TNF-alpha (20 ng mL-1) pretreatment of human antral fragments: basal gastrin release was increased by 38% (P < 0.05) and bombesin-stimulated by 26% (P < 0.05). This effect persisted during immunoblockade with anti-somatostatin antibody S6. We propose that TNF-alpha provides the link between Hp infection and gastrin release and thus contributes to duodenal ulceration.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Dogs
  • Duodenal Ulcer / etiology
  • Gastric Mucosa / cytology
  • Gastric Mucosa / drug effects
  • Gastric Mucosa / metabolism
  • Gastrins / metabolism*
  • Helicobacter Infections / complications
  • Helicobacter Infections / etiology
  • Helicobacter pylori / pathogenicity*
  • Humans
  • In Vitro Techniques
  • Pyloric Antrum / cytology
  • Pyloric Antrum / drug effects*
  • Pyloric Antrum / metabolism*
  • Tumor Necrosis Factor-alpha / pharmacology*
  • Tumor Necrosis Factor-alpha / physiology


  • Gastrins
  • Tumor Necrosis Factor-alpha