Watanabe Tomohiro, Asano Naoki, Kitani Atsushi, Fuss Ivan J, Chiba Tsutomu, Strober Warren
Mucosal Immunity Section, Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10-CRC Room 5W3940, 10 Center Drive, Bethesda, MD 20892, USA.
Int J Inflam. 2010 Jul 15;2010:476482. doi: 10.4061/2010/476482.
Infection of the stomach with Helicobacter pylori is an important risk factor for gastritis, peptic ulcer, and gastric carcinoma. Although it has been well established that persistent colonization by H. pylori is associated with adaptive Th1 responses, the innate immune responses leading to these Th1 responses are poorly defined. Recent studies have shown that the activation of nucleotide-binding oligomerization domain 1 (NOD1) in gastric epithelial cells plays an important role in innate immune responses against H. pylori. The detection of H. pylori-derived ligands by cytosolic NOD1 induces several host defense factors, including antimicrobial peptides, cytokines, and chemokines. In this paper, we review the molecular mechanisms by which NOD1 contributes to mucosal host defense against H. pylori infection of the stomach.
幽门螺杆菌感染胃部是胃炎、消化性溃疡和胃癌的重要危险因素。尽管幽门螺杆菌持续定植与适应性Th1反应相关这一点已得到充分证实,但导致这些Th1反应的固有免疫反应却知之甚少。最近的研究表明,胃上皮细胞中核苷酸结合寡聚化结构域1(NOD1)的激活在针对幽门螺杆菌的固有免疫反应中起重要作用。胞质NOD1对幽门螺杆菌衍生配体的检测可诱导多种宿主防御因子,包括抗菌肽、细胞因子和趋化因子。在本文中,我们综述了NOD1促进黏膜宿主防御胃部幽门螺杆菌感染的分子机制。