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

Fadia R Homaidan1, Iman Chakroun, Marwan E El-Sabban

  • 1Department of Physiology, American University of Beirut, Faculty of Medicine, Beirut, Lebanon. fh01@aub.edu.lb

Mediators of Inflammation
|February 6, 2004
PubMed

Insights

Interleukin-1 (IL-1) activates nuclear factor-kappaB (NF-kappaB) in intestinal cells, influencing inflammation and cell survival. This suggests NF-kappaB is a potential therapeutic target for inflammatory bowel disease.

Area of Science:

  • Cellular and Molecular Biology
  • Immunology
  • Gastroenterology

Background:

  • Interleukin-1 (IL-1) is an inflammatory cytokine found at elevated levels in inflamed mucosa.
  • IL-1 contributes to its effects on intestinal epithelial cells (IEC) by inducing ceramide production.

Purpose of the Study:

  • To investigate the role of nuclear factor-kappaB (NF-kappaB) in IL-1-treated IEC.
  • NF-kappaB is recognized as a pro-inflammatory and anti-apoptotic factor.

Main Methods:

  • Assessed NF-kappaB activity using electrophoretic mobility shift assay.
  • Quantified levels of apoptotic proteins via RNA-protection assay.

Main Results:

  • IL-1 and ceramide significantly activated NF-kappaB levels in IEC.
  • Activation of NF-kappaB correlated with decreased IkappaB-alpha and IkappaB-beta protein levels.
  • IL-1 treatment led to a significant increase in the ratio of anti-apoptotic to pro-apoptotic mRNA in IEC.

Conclusions:

  • NF-kappaB plays a crucial role in regulating pro-inflammatory and/or apoptotic gene expression.
  • NF-kappaB represents an attractive therapeutic target for inflammatory bowel disease (IBD).
Abstract

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