Exposure of intestinal epithelial cell HT29 to bile acids and ammonia enhances Mac-1-mediated neutrophil adhesion

1999 ◽  
Vol 48 (5) ◽  
pp. 265-273 ◽  
Author(s):  
R. Miyata ◽  
K. Iwabuchi ◽  
S. Watanabe ◽  
N. Sato ◽  
I. Nagaoka
Keyword(s):  
Epithelial Cell ◽  
Bile Acids ◽  
Intestinal Epithelial Cell ◽  
Neutrophil Adhesion ◽  
Intestinal Epithelial

scholarly journals Bile acids regulate intestinal cell proliferation by modulating EGFR and FXR signaling

2016 ◽  
Vol 310 (2) ◽  
pp. G81-G92 ◽  
Author(s):  
Avafia Y. Dossa ◽  
Oswaldo Escobar ◽  
Jamie Golden ◽  
Mark R. Frey ◽  
Henri R. Ford ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Bile Acids ◽  
Intestinal Epithelial Cell ◽  
Enteric Bacteria ◽  
Intestinal Cell ◽  
Intestinal Epithelial ◽  
Epithelial Cell Proliferation ◽  
Inhibition Of Proliferation ◽  
Genetic Ablation

Bile acids (BAs) are synthesized in the liver and secreted into the intestine. In the lumen, enteric bacteria metabolize BAs from conjugated, primary forms into more toxic unconjugated, secondary metabolites. Secondary BAs can be injurious to the intestine and may contribute to disease. The epidermal growth factor receptor (EGFR) and the nuclear farnesoid X receptor (FXR) are known to interact with BAs. In this study we examined the effects of BAs on intestinal epithelial cell proliferation and investigated the possible roles for EGFR and FXR in these effects. We report that taurine-conjugated cholic acid (TCA) induced proliferation, while its unconjugated secondary counterpart deoxycholic acid (DCA) inhibited proliferation. TCA stimulated phosphorylation of Src, EGFR, and ERK 1/2. Pharmacological blockade of any of these pathways or genetic ablation of EGFR abrogated TCA-stimulated proliferation. Interestingly, Src or EGFR inhibitors eliminated TCA-induced phosphorylation of both molecules, suggesting that their activation is interdependent. In contrast to TCA, DCA exposure diminished EGFR phosphorylation, and pharmacological or siRNA blockade of FXR abolished DCA-induced inhibition of proliferation. Taken together, these results suggest that TCA induces intestinal cell proliferation via Src, EGFR, and ERK activation. In contrast, DCA inhibits proliferation via an FXR-dependent mechanism that may include downstream inactivation of the EGFR/Src/ERK pathway. Since elevated secondary BA levels are the result of specific bacterial modification, this may provide a mechanism through which an altered microbiota contributes to normal or abnormal intestinal epithelial cell proliferation.

Secondary Bile Acids Contribute to Intestinal Epithelial Cell Injury via Inhibition of Cell Migration

2014 ◽  
Vol 219 (3) ◽  
pp. S74
Author(s):  
Stephanie C. Papillon ◽  
Avafia Y. Dossa ◽  
Anne S. Roberts ◽  
Mark R. Frey ◽  
Henri R. Ford ◽  
...  
Keyword(s):  
Cell Migration ◽  
Epithelial Cell ◽  
Bile Acids ◽  
Intestinal Epithelial Cell ◽  
Cell Injury ◽  
Intestinal Epithelial ◽  
Secondary Bile Acids ◽  
Epithelial Cell Injury
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