BACKGROUND & AIMS: Helicobacter pylori infection in patients who have peptic ulcer disease is associated with altered regulation of gastric secretion, hypergastrinemia, and diminished somatostatin expression in gastric mucosa. Tumor necrosis factor (TNF)-alpha and interleukin (IL)-8 are the predominant cytokines produced in the gastric mucosa of patients with H. pylori infection. The aim of this study was to examine whether IL-8 and TNF-alpha could regulate somatostatin release from isolated canine gastric D cells. METHODS: Canine gastric D cells were isolated from fundic mucosa and enriched by centrifugal elutriation. Secretagogue-stimulated somatostatin release was measured by radioimmunoassay. RESULTS: TNF-alpha dose dependently increased somatostatin release after 2 hours of treatment. The stimulatory effect of TNF-alpha was additive to that of epinephrine but was unaffected by a maximal concentration of cholecystokinin. IL-8 did not alter basal or secretagogue (cholecystokinin, epinephrine)-mediated somatostatin release. The stimulatory effect of TNF-alpha (10 ng/mL) was potentiated by the addition of IL-8 (1 nmol/L), inhibited by octreotide and staurosporine, but unaffected by indomethacin. Pretreatment of D cells with TNF-alpha (10 ng/mL) for 24 hours abolished the subsequent stimulatory effect of this cytokine and secretagogues on somatostatin release. CONCLUSIONS: TNF-alpha was shown to regulate somatostatin release from cultured D cells in a divergent manner.
BACKGROUND & AIMS:Helicobacter pyloriinfection in patients who have peptic ulcer disease is associated with altered regulation of gastric secretion, hypergastrinemia, and diminished somatostatin expression in gastric mucosa. Tumor necrosis factor (TNF)-alpha and interleukin (IL)-8 are the predominant cytokines produced in the gastric mucosa of patients with H. pyloriinfection. The aim of this study was to examine whether IL-8 and TNF-alpha could regulate somatostatin release from isolated canine gastric D cells. METHODS:Canine gastric D cells were isolated from fundic mucosa and enriched by centrifugal elutriation. Secretagogue-stimulated somatostatin release was measured by radioimmunoassay. RESULTS:TNF-alpha dose dependently increased somatostatin release after 2 hours of treatment. The stimulatory effect of TNF-alpha was additive to that of epinephrine but was unaffected by a maximal concentration of cholecystokinin. IL-8 did not alter basal or secretagogue (cholecystokinin, epinephrine)-mediated somatostatin release. The stimulatory effect of TNF-alpha (10 ng/mL) was potentiated by the addition of IL-8 (1 nmol/L), inhibited by octreotide and staurosporine, but unaffected by indomethacin. Pretreatment of D cells with TNF-alpha (10 ng/mL) for 24 hours abolished the subsequent stimulatory effect of this cytokine and secretagogues on somatostatin release. CONCLUSIONS:TNF-alpha was shown to regulate somatostatin release from cultured D cells in a divergent manner.
Authors: T Fukui; A Nishio; K Okazaki; N Uza; S Ueno; M Kido; S Inoue; H Kitamura; K Kiriya; S Ohashi; M Asada; H Tamaki; M Matsuura; K Kawasaki; K Suzuki; K Uchida; H Fukui; H Nakase; N Watanabe; T Chiba Journal: Gut Date: 2005-12-01 Impact factor: 23.059
Authors: Jesper A B Strickertsson; Kristina B V Døssing; Anna J M Aabakke; Hans-Olof Nilsson; Thomas V O Hansen; Ulrich Knigge; Andreas Kjær; Torkel Wadström; Lennart Friis-Hansen Journal: World J Gastroenterol Date: 2011-07-14 Impact factor: 5.742
Authors: Yana Zavros; Sivaprakash Rathinavelu; John Y Kao; Andrea Todisco; John Del Valle; Joel V Weinstock; Malcolm J Low; Juanita L Merchant Journal: Proc Natl Acad Sci U S A Date: 2003-10-10 Impact factor: 11.205