scholarly journals Tumor necrosis factor α decreases aquaporin 3 expression in intestinal epithelial cells through inhibition of constitutive transcription

2017 ◽  
Vol 5 (19) ◽  
pp. e13451 ◽  
Author(s):  
Michael A. Peplowski ◽  
Andrew J. Vegso ◽  
Vadim Iablokov ◽  
Michael Dicay ◽  
Raza S. Zaheer ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Aquaporin 3 ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Activation of muscarinic cholinoceptor ameliorates tumor necrosis factor-α-induced barrier dysfunction in intestinal epithelial cells

FEBS Letters ◽  
2015 ◽  
Vol 589 (23) ◽  
pp. 3640-3647 ◽  
Author(s):  
Md Rafiqul Islam Khan ◽  
Junsuke Uwada ◽  
Takashi Yazawa ◽  
Md Tariqul Islam ◽  
Susanne M. Krug ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Factor Α ◽  
Necrosis Factor

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.

scholarly journals Regulation of NF-κB responses by epigenetic suppression of IκBα expression in HCT116 intestinal epithelial cells

2010 ◽  
Vol 299 (1) ◽  
pp. G96-G105 ◽  
Author(s):  
Angela O'Gorman ◽  
Amy Colleran ◽  
Aideen Ryan ◽  
Jelena Mann ◽  
Laurence John Egan
Keyword(s):  
Epithelial Cells ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Intestinal Epithelial Cells ◽  
Gene Promoter ◽  
Intestinal Epithelial ◽  
Epigenetic Factors ◽  
Factor Α ◽  
Necrosis Factor ◽  
Hct116 Cells

Intestinal epithelial cells play critical roles in regulating mucosal immunity. Since epigenetic factors such as DNA methylation and histone modifications are implicated in aging, carcinogenesis, and immunity, we set out to assess any role for epigenetic factors in the regulation of intestinal epithelial cell immune responses. Experiments were conducted using the HCT116 cell line, and a subclone was genetically engineered to lack DNA methyltransferases (DNMT). The induction of the chemokine interleukin-8 and the antiapoptotic protein cFLIP by tumor necrosis factor-α were markedly less in HCT116 cells lacking DNMT than in parental cells. These effects were accompanied by lower monocyte chemotaxis and higher caspase signaling in HCT116 cells lacking DNMT than parental cells. Tumor necrosis factor-α-induced NF-κB activation was blocked and IκBα expression was higher in HCT116 cells lacking DNMT than in parental cells. A CpG island in the IκBα gene promoter region was found to contain variable levels of methylation in parental HCT116 cells. Chromatin immunoprecipitation analysis of histone proteins bound to the IκBα gene promoter revealed that higher levels of IκBα expression in HCT116 cells lacking DNMT compared with parental cells were accompanied by more chromatin marks permissive to gene transcription. These findings show that epigenetic factors influence the NF-κB system in intestinal epithelial cells, resulting in a previously unrecognized mechanism of innate immune regulation.

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