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Updated: May 5, 2026
10:22
In Vitro and In Vivo Approaches to Determine Intestinal Epithelial Cell Permeability
Published on: October 19, 2018
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Glucocorticoids regulate barrier function and claudin expression in intestinal epithelial cells via MKP-1
Andreas Fischer1, Markus Gluth, Friderike Weege
1Department of Medicine, Division of Gastroenterology and Hepatology Campus Virchow Klinikum and.
Summary
Glucocorticoids enhance intestinal barrier function by increasing specific tight junction proteins, a mechanism that may contribute to their therapeutic effects in inflammatory bowel diseases and collagenous colitis.
Area of Science:
- Gastroenterology
- Cell Biology
- Pharmacology
Background:
- Intestinal barrier dysfunction is central to inflammatory bowel diseases (IBD) and collagenous colitis.
- Glucocorticoids are used to treat Crohn's disease, but their mechanism, particularly epithelial effects, is unclear.
Purpose of the Study:
- To investigate the epithelial-specific effects of glucocorticoids on intestinal barrier function.
- To determine the molecular mechanisms underlying glucocorticoid-induced barrier enhancement.
Main Methods:
- Utilized Caco-2 cell monolayers as an in vitro model of the intestinal epithelial barrier.
- Assessed transepithelial electrical resistance (TEER), solute flux, and tight junction protein expression (claudins, occludin).
- Investigated the role of MAPK phosphatase-1, p38, and MEK1/2 pathways.
Main Results:
- Glucocorticoids increased TEER in a time- and dose-dependent, glucocorticoid receptor-dependent manner.
- This was associated with reduced claudin-2 expression and increased claudin-4 expression.
- Glucocorticoids increased MAPK phosphatase-1 activity, and its inhibition blocked barrier changes; cytokine exposure reduced TEER but remained higher than controls.
Conclusions:
- Glucocorticoids augment intestinal epithelial barrier function independently of reducing inflammation.
- This barrier enhancement, mediated by changes in claudin expression, may be a key therapeutic mechanism in IBD and collagenous colitis.
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