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Int J Med Microbiol. 2010 Jan;300(1):49-56. doi: 10.1016/j.ijmm.2009.08.007. Epub 2009 Sep 24.

Role of NF-kappaB activation in intestinal immune homeostasis.

Author information

1
Department of Mouse Genetics and Inflammation, Institute for Genetics, University of Cologne, Z├╝lpicher Strasse, 47, D-50674 Cologne, Germany. awullaer@uni-koeln.de

Abstract

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.

PMID:
19781989
DOI:
10.1016/j.ijmm.2009.08.007
[Indexed for MEDLINE]

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