Tumour necrosis factor alpha stimulates gastrin release from canine and human antral G cells: possible mechanism of the Helicobacter pylori–gastrin link |
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Authors: | I. L. P. Beales,,L. Post,,J. Calam,,T. Yamada,& J. DelValle |
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Affiliation: | Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London, and;Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA |
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Abstract: | 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. |
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Keywords: | Gastrin Helicobacte r pylori tumour necrosis factor alpha |
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