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Related Concept Videos

Tight Junctions01:29

Tight Junctions

Tight junctions are molecular seals between cells that prevent the leaking of fluids, ions, and other small solutes across cavities and compartments in multicellular organisms. They are mainly composed of claudin and occludin transmembrane proteins, and other proteins such as tricellulin and JAM (junctional adhesion molecule). All these proteins are 4-pass transmembrane proteins, except JAM, which is a single-pass transmembrane protein belonging to the immunoglobulin superfamily. The...
Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
Adherens Junctions01:24

Adherens Junctions

Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
Adherens Junctions are Dynamic
The endothelial cells...
Renewal of Intestinal Stem Cells01:23

Renewal of Intestinal Stem Cells

The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the goblet,...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...

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Related Experiment Video

Updated: Jun 22, 2026

Sensing of Barrier Tissue Disruption with an Organic Electrochemical Transistor
11:17

Sensing of Barrier Tissue Disruption with an Organic Electrochemical Transistor

Published on: February 10, 2014

Epithelial tight junctions in intestinal inflammation.

Joerg D Schulzke1, Svenja Ploeger, Maren Amasheh

  • 1Department of General Medicine & Pathophysiology of Enteral Nutrition, Charité, Campus Benjamin Franklin, Berlin, Germany. joerg.schulzke@charite.de

Annals of the New York Academy of Sciences
|June 23, 2009
PubMed
Summary

Inflammatory bowel diseases (IBD) like Crohn's disease and ulcerative colitis involve intestinal barrier defects. Cytokines disrupt epithelial tight junctions, increase apoptosis, and affect antigen transport, leading to diarrhea and inflammation.

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Functional Assessment of Intestinal Tight Junction Barrier and Ion Permeability in Native Tissue by Ussing Chamber Technique
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Functional Assessment of Intestinal Tight Junction Barrier and Ion Permeability in Native Tissue by Ussing Chamber Technique

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Last Updated: Jun 22, 2026

Sensing of Barrier Tissue Disruption with an Organic Electrochemical Transistor
11:17

Sensing of Barrier Tissue Disruption with an Organic Electrochemical Transistor

Published on: February 10, 2014

Functional Assessment of Intestinal Tight Junction Barrier and Ion Permeability in Native Tissue by Ussing Chamber Technique
06:43

Functional Assessment of Intestinal Tight Junction Barrier and Ion Permeability in Native Tissue by Ussing Chamber Technique

Published on: May 26, 2021

Area of Science:

  • Gastroenterology
  • Immunology
  • Cell Biology

Background:

  • Intestinal epithelial barrier integrity is crucial for gut homeostasis.
  • Inflammatory bowel diseases (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), are characterized by compromised intestinal barrier function.
  • Specific molecular and cellular mechanisms underlying barrier defects in IBD require further elucidation.

Purpose of the Study:

  • To delineate the distinct mechanisms of epithelial barrier disruption in Crohn's disease and ulcerative colitis.
  • To investigate the role of cytokines, tight junctions, apoptosis, and microbial factors in IBD pathogenesis.
  • To understand how barrier dysfunction contributes to symptoms like diarrhea and mucosal inflammation.

Main Methods:

  • Analysis of epithelial changes in inflamed intestinal tissues from IBD patients.
  • Assessment of tight junction protein alterations.
  • Evaluation of epithelial apoptosis and its contribution to barrier defects.
  • Investigation of cytokine profiles (IFN-gamma, TNF-alpha, IL-13) and their effects on epithelial cells.
  • Consideration of microbial factors, such as alpha-hemolysin-producing E. coli.

Main Results:

  • Crohn's disease shows reduced tight junction strands and altered protein composition.
  • Ulcerative colitis exhibits early epithelial leaks due to apoptosis and increased claudin-2 expression.
  • Interferon-gamma and TNF-alpha drive epithelial damage in CD; IL-13 is key in UC.
  • Focal lesions from apoptotic cells and alpha-hemolysin-producing E. coli contribute to barrier disturbance.
  • Pro-inflammatory cytokines exacerbate transcellular antigen translocation, potentially initiating IBD.

Conclusions:

  • Distinct cytokine-driven mechanisms impair the intestinal epithelial barrier in CD and UC.
  • Barrier defects, including tight junction dysfunction and apoptosis, promote leak flux diarrhea and antigen uptake in IBD.
  • Immune regulation of epithelial cells by cytokines plays a central role in IBD pathogenesis through multiple barrier-disrupting pathways.