幽门螺杆菌定植胃中胃饥饿素合成受损：幽门螺杆菌相关胃炎症发病机制的新线索
Impairment of ghrelin synthesis in Helicobacter pylori-colonized stomach: new clues for the pathogenesis of H. pylori-related gastric inflammation.
作者信息
Paoluzi Omero Alessandro, Blanco Del Vecchio Giovanna, Caruso Roberta, Monteleone Ivan, Monteleone Giovanni, Pallone Francesco
机构信息
Omero Alessandro Paoluzi, Giovanna Del Vecchio Blanco, Roberta Caruso, Ivan Monteleone, Giovanni Monteleone, Francesco Pallone, Department of Systems Medicine, University of Rome "Tor Vergata", 00133 Rome, Italy.
出版信息
World J Gastroenterol. 2014 Jan 21;20(3):639-46. doi: 10.3748/wjg.v20.i3.639.
Ghrelin, the ligand of growth hormone secretagogue receptor 1a, takes part in several functions of the digestive system, including regulation of appetite, energy homeostasis, gastric acid secretion and motility. Ghrelin has also immunoregulatory properties and is supposed to inhibit some inflammatory pathways that can mediate gastric damage. Interestingly, ghrelin synthesis is reduced in the gastric mucosa of patients with Helicobacter pylori (H. pylori) infection, a worldwide condition inducing a T helper (Th)1/Th17 cell response-driven gastritis, which may evolve towards gastric atrophy and cancer. In this article, we review the available data on the expression of ghrelin in H. pylori infection and discuss how the defective ghrelin synthesis may contribute to sustain the ongoing inflammatory response in this disease.
胃饥饿素是生长激素促分泌素受体1a的配体，参与消化系统的多种功能，包括食欲调节、能量平衡、胃酸分泌和胃肠蠕动。胃饥饿素还具有免疫调节特性，被认为可抑制一些能介导胃损伤的炎症途径。有趣的是，在幽门螺杆菌（H. pylori）感染患者的胃黏膜中，胃饥饿素的合成减少。幽门螺杆菌感染是一种全球性疾病，可引发由辅助性T细胞（Th）1/Th17细胞反应驱动的胃炎，这种胃炎可能会发展为胃萎缩和癌症。在本文中，我们综述了幽门螺杆菌感染中胃饥饿素表达的现有数据，并讨论了胃饥饿素合成缺陷可能如何导致该疾病中持续的炎症反应。
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