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

2003 ◽  
Vol 12 (5) ◽  
pp. 277-283 ◽  
Author(s):  
Fadia R. Homaidan ◽  
Iman Chakroun ◽  
Marwan E. El-sabban
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Cell Model ◽  
Interleukin 1 ◽  
Nuclear Factor Κb ◽  
Mrna Levels ◽  
Nuclear Factor ◽  
Intestinal Epithelial ◽  
Mobility Shift ◽  
Apoptotic Proteins

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.

scholarly journals Polo-like kinase 1 protects intestinal epithelial cells from apoptosis during sepsis via the nuclear factor-κB pathway

2020 ◽  
Vol 133 (15) ◽  
pp. 1886-1888
Author(s):  
Ying-Ya Cao ◽  
Zhen Wang ◽  
Lin-Ming Lu ◽  
Zeng-Xiang Xu ◽  
Jia-Jia Li ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Intestinal Epithelial

Developmentally regulated tumor necrosis factor-α induced nuclear factor-κB activation in intestinal epithelium

2007 ◽  
Vol 292 (5) ◽  
pp. G1411-G1419 ◽  
Author(s):  
Erika C. Claud ◽  
Xiaoqiong Zhang ◽  
Elaine O. Petrof ◽  
Jun Sun
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Intestinal Epithelial Cells ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Intestinal Epithelial ◽  
Factor Α ◽  
Necrosis Factor

Premature infants are susceptible to many conditions that are inflammatory in nature. For this patient population, which is expecting the intrauterine environment, pathways necessary for fetal life and development may not have completed the transitions necessary for extrauterine life. In this study, responses to tumor necrosis factor-α were compared in human fetal and adult intestinal epithelial cell lines along with preweaned and postweaned mouse intestinal sections to identify a potential developmental difference that may explain the heightened inflammatory response of preterm infants. The nuclear factor-κB (NF-κB) pathway regulates a wide variety of genes involved in immune and inflammatory processes. We report that, compared with adult intestinal epithelial cells, immature intestinal epithelial cells have increased NF-κB activity associated with increased NF-κB-DNA binding and transcriptional activity. This increased activity appears due to inadequate inhibition of signaling leading to NF-κB activation since there is also increased phosphorylation, ubiquitination, and degradation of the inhibitor of NF-κB in conjunction with decreased baseline expression and delayed resynthesis of this inhibitor. Thus we demonstrate a potential mechanism for the heightened inflammatory response of immature intestinal epithelial cells.

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