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Am J Physiol Gastrointest Liver Physiol (October 21, 2004). doi:10.1152/ajpgi.00377.2004
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Submitted on August 17, 2004
Accepted on October 10, 2004

Toll-like receptor-mediated responses of primary intestinal epithelial cells during the development of colitis

Joy Carmelina Indira Singh1, Sheena Margaret Cruickshank1, Darren James Newton1, Louise Wakenshaw1, Anne Graham1, Jinggang Lan1, Jeremy Peter Alan Lodge2, Peter John Felsburg3, and Simon Richard Carding1*

1 School of Biochemistry and Microbiology, The University of Leeds, Leeds, W. Yorks, United Kingdom
2 General Surgery, Medicine and Anaesthesia, School of Medicine, The University of Leeds, Leeds, W. Yorks, United Kingdom
3 Department of Clinical Studies, University of Pennsylvania school of Veterinary Medicine, Philadelphia, Pennsylvania, USA

* To whom correspondence should be addressed. E-mail: S.R.Carding{at}Leeds.ac.uk.

The interleukin-2 (IL-2)-deficient (IL-2-/-) mouse model of ulcerative colitis was used to test the hypothesis that colonic epithelial cells (CEC) directly respond to bacterial antigens and that alterations in Toll-like receptor- (TLR) mediated signaling may occur during the development of colitis. TLR expression and activation of TLR-mediated signaling pathways in primary CEC of healthy animals was compared with CEC in IL2-/- mice during the development of colitis. In healthy animals, CEC expressed functional TLR and in response to the TLR4 ligand, lipopolysaccharide (LPS), proliferated and secreted the cytokines, IL-6 and MCP-1. However, the TLR-responsiveness of CEC in IL-2-/- mice was different with decreased TLR4 responsiveness and augmented TLR2 responses that result in IL-6 and MCP-1 secretion. TLR signaling in CEC did not involve NF-{kappa}B (p65) activation with the inhibitory p50 form of NF-{kappa}B predominating in CEC in both the healthy and inflamed colon. The development of colitis was however associated with the activation of MAPK family members and upregulation of MyD88-independent signaling pathways characterized by increased caspase-1 activity and IL-18 production. These findings identify changes in TLR expression and signaling during the development of colitis that may contribute to changes in the host response to bacterial antigens seen in colitis.




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