Department of Mouse Genetics and Inflammation, Institute for Genetics, University of Cologne, Zülpicher Strasse, 47, D-50674 Cologne, Germany.
Int J Med Microbiol. 2010 Jan;300(1):49-56. doi: 10.1016/j.ijmm.2009.08.007. Epub 2009 Sep 24.
Inflammatory bowel diseases (IBD) are characterised by a disturbance of intestinal immune homeostasis, either caused by or followed by inappropriate responses to the resident commensal bacteria. Although the transcription factor NF-kappaB actively participates in the excessive inflammatory response observed in IBD, recent studies with mice defective in NF-kappaB activation have revealed that NF-kappaB also serves an essential protective function in the intestinal immune system. The enormous amount of commensal bacteria in the intestine might play a role in the distinct functions of NF-kappaB in the intestine, as they can initiate signalling to NF-kappaB through both Toll-like receptors and NOD-like receptors in intestinal epithelial cells as well as mucosal immune cells. However, the exact individual contributions of different NF-kappaB-activating stimuli as well as the target cells that mediate the detrimental or beneficial functions of NF-kappaB in the intestine are still elusive. In this review, I will summarise and discuss the current knowledge on the role of different NF-kappaB-activating pathways in preserving intestinal immune homeostasis and the development of intestinal inflammation.
炎症性肠病(IBD)的特征是肠道免疫稳态紊乱,这种紊乱要么是由常驻共生细菌引起的,要么是对其产生不适当反应的结果。尽管转录因子 NF-κB 积极参与 IBD 中观察到的过度炎症反应,但最近对 NF-κB 激活有缺陷的小鼠的研究表明,NF-κB 也在肠道免疫系统中发挥着重要的保护功能。肠道中大量的共生细菌可能在 NF-κB 在肠道中的不同功能中发挥作用,因为它们可以通过 Toll 样受体和 NOD 样受体在肠道上皮细胞以及黏膜免疫细胞中向 NF-κB 发出信号。然而,不同 NF-κB 激活刺激物的具体个体贡献以及介导 NF-κB 在肠道中发挥有害或有益功能的靶细胞仍不清楚。在这篇综述中,我将总结和讨论不同 NF-κB 激活途径在维持肠道免疫稳态和肠道炎症发展中的作用的现有知识。