Role of NF-kappaB activation in intestinal immune homeostasis.
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.
Department of Mouse Genetics and Inflammation, Institute for Genetics, University of Cologne, Zülpicher Strasse, 47, D-50674 Cologne, Germany. awullaer@uni-koeln.de
Andy
A
Wullaert
D000818:Animals; D001419:Bacteria / Q000276:immunology*; D006706:Homeostasis; D006801:Humans; D007108:Immune Tolerance; D007109:Immunity; D007422:Intestines / Q000276:immunology* / Q000382:microbiology*; D051379:Mice; D016328:NF-kappa B / Q000276:immunology*
D016328:NF-kappa B