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Tumour necrosis factor alpha stimulates gastrin release from canine and human antral G cells: possible mechanism of the Helicobacter pylori –gastrin link
Author(s) -
Beales I. L. P.,
Post L.,
Calam J.,
Yamada T.,
DelValle J.
Publication year - 1996
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1996.2040517.x
Subject(s) - gastrin , medicine , g cell , endocrinology , bombesin , helicobacter pylori , antrum , somatostatin , tumor necrosis factor alpha , pyloric antrum , basal (medicine) , peptide hormone , biology , hormone , stomach , neuropeptide , secretion , receptor , insulin
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‐α) 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‐α pretreatment (100ngmL –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‐α (20ngmL −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‐α provides the link between Hp infection and gastrin release and thus contributes to duodenal ulceration.