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Updated: Jun 12, 2026

Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids
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Context-Dependent Epithelial and Immune Programs Shape Intestinal Resilience or Vulnerability Following Prior

Priyanka Biswas1, Vishwas Mishra1, Julia Sanchez-Garrido1

  • 1Department of Life Sciences, Imperial College London, London, United Kingdom.

Cellular and Molecular Gastroenterology and Hepatology
|June 10, 2026
PubMed
Summary
This summary is machine-generated.

Prior infectious colitis confers protection against subsequent sterile colitis by maintaining gut barrier integrity. However, sterile colitis leads to persistent barrier defects, increasing susceptibility to infection. This highlights how inflammatory history impacts intestinal resilience.

Keywords:
C rodentiumDSS ColitisEnteropathogenic Escherichia coliEpithelial Barrier IntegrityIL17AInflammatory MemoryMucosal ImmunityType III Secretion System Effectors

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Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells
06:57

Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells

Published on: September 18, 2016

Area of Science:

  • Gastroenterology
  • Immunology
  • Microbiology

Background:

  • Prior intestinal inflammation can alter immune and epithelial responses to subsequent injury.
  • Infectious and sterile colitis share features like barrier disruption and cytokine secretion.
  • The influence of initial inflammatory events on subsequent disease outcomes is not fully understood.

Purpose of the Study:

  • To investigate if the type of initial colitis (infectious vs. sterile) affects protection or susceptibility to secondary intestinal insult.
  • To define how prior infectious versus sterile colitis shapes secondary disease progression.

Main Methods:

  • Reciprocal mouse models of Citrobacter rodentium (CR) infection and dextran sodium sulphate (DSS)-induced colitis were employed.
  • Assessed barrier integrity, immune cell populations, cytokine production, and susceptibility to wild-type and CR mutants.
  • Evaluated the role of type III secretion system effectors and IL-17A signaling.

Main Results:

  • Mice recovered from CR infection were protected against DSS colitis, showing reduced pathology and preserved epithelial architecture.
  • Protection after CR infection was linked to sustained IL-17A signaling and required type III secretion system effectors.
  • Mice recovered from DSS colitis had persistent barrier defects and were more susceptible to CR infection, even with minimal epithelial damage.

Conclusions:

  • The nature of primary colitis establishes distinct, persistent epithelial and immune programs.
  • Infectious colitis promotes a protective mucosal state, with IL-17A as a key contributor.
  • Sterile colitis results in epithelial barrier dysfunction, increasing susceptibility to subsequent infections, highlighting the impact of inflammatory history on intestinal resilience.