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Updated: Apr 15, 2026

An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
Published on: December 3, 2020
Changes in Epithelial Barrier Function in Response to Parasitic Infection: Implications for IBD Pathogenesis
Joan Antoni Fernández-Blanco1, Javier Estévez1, Terez Shea-Donohue2
1Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, Barcelona, Spain.
Following gut infection, mast cell proteinases and altered tight junction proteins increase gut permeability. This study tracks these changes in a rat model, revealing mechanisms for post-infectious gut dysfunction.
Area of Science:
- Gastroenterology
- Immunology
- Cell Biology
Background:
- Mast cells (MCs) are involved in epithelial barrier dysfunction in inflammatory bowel diseases.
- Mast cell proteinases and tight junction (TJ) proteins play roles in gut barrier integrity.
Purpose of the Study:
- To investigate the kinetics of mast cell proteinases and TJ proteins in a rat model of postinfectious gut dysfunction.
- To elucidate the molecular mechanisms underlying epithelial barrier alterations after gut infection.
Main Methods:
- Jejunal tissues from control and infected rats were analyzed.
- Immunostaining and RT-qPCR were used to assess MCs and TJ protein expression.
- Epithelial barrier function was evaluated using in vitro (Ussing chambers) and in vivo models.
Main Results:
- Intestinal inflammation led to overexpression of MC chymases and hyperplasia.
- Down-regulation of occludin and claudin-3, with overexpression of claudin-2, was observed post-infection.
- Reduced proglucagon expression and increased epithelial permeability were associated with these molecular changes.
Conclusions:
- Mast cell proteinase expression and localization follow a time-dependent pattern post-infection.
- Altered TJ protein expression contributes to reduced epithelial tightness and increased permeability.
- These findings provide a molecular basis for post-infectious gut barrier dysfunction.
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