Gastrin secretion from primary cultures of rabbit antral G cells: Stimulation by inflammatory cytokines
Gastrin secretion from primary cultures of rabbit antral G cells: Stimulation by inflammatory cytokines
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DOI：
10.1053/gast.1996.v110.pm8536851
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发表时间：
1996-01-01
期刊：
影响因子：
29.4
通讯作者：
Schepp, W
中科院分区：
文献类型：
--
作者：
Weigert, N;Schaffer, K;Schepp, W
背景与目的：在幽门螺杆菌诱导的胃炎中，局部细胞因子的产生可能有利于高胃泌素血症，这是幽门螺杆菌与胃粘膜炎症之间的内分泌联系。幽门引起的胃炎和十二指肠溃疡。本研究的目的是表征细胞因子对培养的兔胃窦G细胞的影响。方法：在原代培养48小时后研究单层（14.2% +/- 2.9% G细胞）。结果如下：白细胞介素（IL）1 β（50%有效浓度[EC（50）]，5.3 +/- 0.4 ng/mL）和肿瘤坏死因子（TNF）α（EC（50），5.5 +/- 0.5 ng/mL）刺激胃泌素释放至10（-9）mol/L神经介肽C最大反应的50%。人IL-1受体拮抗剂（100 ng/mL抑制常数，23.0 ng/mL）可抑制最大有效浓度的IL-1 β（10 ng/mL）的刺激作用，其偏好I型IL-1受体而非II型IL-1受体。对TNF-α最大有效浓度的反应TNF P55受体拮抗剂单克隆抗体H398（10 ng/mL）可显著抑制TNF P55的表达（抑制常数，1.7 μ g/mL），而TNF P75受体拮抗剂单克隆抗体utr 1无效，IL-1 β和TNF-α的刺激可增加对神经介肽C和O-2-二丁酰腺苷3 '，5'-环一磷酸的反应。IL-6和IL-8（0.1-50 ng/mL）无效。结论：IL-1 β和TNF-α通过可能存在于兔胃窦G细胞自身的受体刺激胃泌素分泌。我们推测0细胞表达I型IL-1受体和TNF-P55受体，但不表达TNF-P75受体。
Background & Aims: In Helicobacter pylori-induced gastritis, local production of cytokines may favor hypergastrinemia as an endocrine link between H. pylori-induced gastritis and duodenal ulcer. The aim of this study was to characterize cytokine effects on cultured rabbit antral G cells. Methods: Monolayers (14.2% +/- 2.9% G cells) were studied after 48 hours in primary culture. Results: Interleukin (IL) 1 beta (50% effective concentration [EC(50)], 5.3 +/- 0.4 ng/mL) and tumor necrosis factor (TNF) alpha (EC(50), 5.5 +/- 0.5 ng/mL) stimulated gastrin release to 50% of the maximal response to 10(-9) mol/L neuromedin C. Stimulation by the maximally effective concentration of IL-1 beta (10 ng/mL) was inhibited by the human IL-1 receptor antagonist (100 ng/mL inhibitory constant, 23.0 ng/mL), which prefers type I over type II IL-1 receptors. The response to the maximally effective concentration of TNF-alpha (10 ng/mL) was markedly inhibited by monoclonal antibody H398, an antagonist at TNF P55 receptors (inhibitory constant, 1.7 mu g/mL), whereas monoclonal antibody utr1, an antagonist at TNF P75 receptors, was ineffective, Stimulation by IL-1 beta and TNF-alpha was additive to the responses to neuromedin C and O-2-dibutyryl adenosine 3',5'-cyclic monophosphate. IL-6 and IL-8 (0.1-50 ng/mL) were ineffective, Conclusions: IL-1 beta and TNF-alpha stimulate gastrin secretion via receptors potentially residing on rabbit antral G cells themselves, We speculate that 0 cells express type I IL-1 receptors and TNF P55 but not TNF P75 receptors.