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幽门螺杆菌增强胆汁酸诱导的大鼠浆膜肥大细胞组胺释放。

Helicobacter pylori potentiates histamine release from rat serosal mast cells induced by bile acids.

作者信息

Masini E, Bechi P, Dei R, Di Bello M G, Sacchi T B

机构信息

Dipartimenti di Farmacologia Preclinica e Clinica, Università di Firenze, Italy.

出版信息

Dig Dis Sci. 1994 Jul;39(7):1493-500. doi: 10.1007/BF02088054.

Abstract

In the present study we have experimentally addressed the effects of Helicobacter pylori on the bile acid capability of histamine release. Bile acids alone were confirmed to be able to induce in vitro histamine release from rat serosal and mucosal mast cells. On the contrary, no significant histamine release was obtained when incubating any Helicobacter pylori preparations alone with mast cells. However, histamine release induced by bile acids was significantly enhanced, without any significant increase in lactate dehydrogenase activity, when whole washed or formalin-killed bacterial cells or crude cell walls were incubated with mast cells in the presence of cholic (0.3 mM), deoxycholic (0.3 mM), or lithocholic (0.3 mM) acids, chenodeoxycholylglycine (0.3 mM), and deoxycholyltaurine (3 mM). The electron microscopic features of mast cells incubated with Helicobacter pylori were consistent with an exocytotic secretion. The release of histamine induced by 0.3 mM deoxycholic acid in the presence of Helicobacter pylori was inhibited by the preincubation of the cells with dimaprit (an H2 agonist) and potentiated by the H2 antagonist, ranitidine. The current results suggest a link between human Helicobacter pylori infection and histamine release and a possible involvement of gastric mucosal mast cells in the pathogenesis of Helicobacter pylori-associated gastritis.

摘要

在本研究中,我们通过实验探讨了幽门螺杆菌对组胺释放胆汁酸能力的影响。单独的胆汁酸被证实能够在体外诱导大鼠浆膜和黏膜肥大细胞释放组胺。相反,当单独将任何幽门螺杆菌制剂与肥大细胞一起孵育时,未获得明显的组胺释放。然而,当在胆酸(0.3 mM)、脱氧胆酸(0.3 mM)或石胆酸(0.3 mM)、鹅去氧胆酰甘氨酸(0.3 mM)和脱氧胆酰牛磺酸(3 mM)存在的情况下,将全菌洗涤或福尔马林灭活的细菌细胞或粗细胞壁与肥大细胞一起孵育时,胆汁酸诱导的组胺释放显著增强,而乳酸脱氢酶活性没有任何显著增加。与幽门螺杆菌一起孵育的肥大细胞的电子显微镜特征与胞吐分泌一致。在幽门螺杆菌存在的情况下,0.3 mM脱氧胆酸诱导的组胺释放被细胞与二甲双胍(一种H2激动剂)预孵育所抑制,并被H2拮抗剂雷尼替丁增强。目前的结果表明人类幽门螺杆菌感染与组胺释放之间存在联系,并且胃黏膜肥大细胞可能参与幽门螺杆菌相关性胃炎的发病机制。

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