Tumour necrosis factor alpha stimulates gastrin release from canine and human antral G cells: possible mechanism of the Helicobacter pylori-gastrin link.
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.
Beales
I L
IL
Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
Post
L
L
Calam
J
J
Yamada
T
T
Delvalle
J
J
D000818:Animals; D002478:Cells, Cultured; D004285:Dogs; D004381:Duodenal Ulcer / Q000209:etiology; D005753:Gastric Mucosa / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D005755:Gastrins / Q000378:metabolism*; D016481:Helicobacter Infections / Q000150:complications / Q000209:etiology; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D066298:In Vitro Techniques; D011706:Pyloric Antrum / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology* / Q000502:physiology
D005755:Gastrins; D014409:Tumor Necrosis Factor-alpha