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Mediators of Inflammation
Volume 12, Issue 5, Pages 277-283

Regulation of nuclear factor-κB in intestinal epithelial cells in a cell model of inflammation

1Department of Physiology, American University of Beirut, Faculty of Medicine, Beirut, Lebanon
2Department of Human Morphology, American University of Beirut, Faculty of Medicine, Beirut, Lebanon

Copyright © 2003 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background: Interleukin-1 (IL-1), an inflammatory cytokine whose levels are elevated in inflamed mucosa, causes part of its effect on intestinal epithelial cells (IEC) through inducing ceramide production.

Aim: To study the role of nuclear factor-κB (NF-κB), a pro-inflammatory and anti-apoptotic factor, in IL-1- treated IEC.

Methods: NF-κB activity and levels of apoptotic proteins were assessed by electrophoretic mobility shift assay and RNA-protection assay, respectively.

Results: IL-1 and ceramide, which have been shown to partially mediate IL-l effects on IEC, activated NF-κB levels significantly. This activation was due to a decrease in IκB-α and IκB-β protein levels. Moreover, the ratio of mRNA levels of anti-apoptotic to pro-apoptotic proteins was significantly increased in IL-1-treated IEC.

Conclusion: NF-κB may play a key role in the regulation of the expression of pro-inflammatory and/or apoptotic genes in inflammatory bowel disease, making this protein an attractive target for therapeutic intervention.