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Related Concept Videos

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...
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...
Inflammatory Bowel Disease II: Crohn's Disease01:30

Inflammatory Bowel Disease II: Crohn's Disease

Introduction
Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
Crohn's disease is a chronic, systemic inflammatory bowel disease (IBD) that predominantly affects the gastrointestinal tract. It is marked by transmural...
Inflammatory Bowel Disease I: Introduction01:26

Inflammatory Bowel Disease I: Introduction

Inflammatory bowel disease is a group of chronic disorders marked by recurrent inflammation of the gastrointestinal tract due to an abnormal immune response against gut microflora. This leads to tissue damage. The two main forms are Crohn’s disease and ulcerative colitis.Crohn’s DiseaseCrohn’s disease is a relapsing inflammatory disorder that can affect any part of the GI tract, from the mouth to the anus. It involves all layers of the bowel wall (transmural) and shows “skip lesions” in which...
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...

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Related Experiment Video

Updated: Jul 19, 2026

Culture Methods to Study Apical-Specific Interactions using Intestinal Organoid Models
07:49

Culture Methods to Study Apical-Specific Interactions using Intestinal Organoid Models

Published on: March 23, 2021

Inflammatory bowel disease and the apical junctional complex.

Matthias Bruewer1, Stanislav Samarin, Asma Nusrat

  • 1Department of General Surgery, University of Muenster, Muenster 48149, Germany.

Annals of the New York Academy of Sciences
|October 24, 2006
PubMed
Summary

The intestinal barrier, regulated by apical junctional complexes (AJC), is compromised in inflammatory bowel disease (IBD). Proinflammatory cytokines like interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) disrupt AJC structure, increasing intestinal permeability.

Related Experiment Videos

Last Updated: Jul 19, 2026

Culture Methods to Study Apical-Specific Interactions using Intestinal Organoid Models
07:49

Culture Methods to Study Apical-Specific Interactions using Intestinal Organoid Models

Published on: March 23, 2021

Area of Science:

  • Gastroenterology
  • Cell Biology
  • Immunology

Background:

  • The intestinal mucosa forms a critical barrier, regulated by the apical junctional complex (AJC), comprising tight junctions (TJs) and adherens junctions (AJs).
  • This barrier function is compromised in inflammatory bowel disease (IBD), characterized by increased intestinal permeability.
  • Proinflammatory cytokines, such as interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), are elevated in IBD and implicated in barrier dysfunction.

Purpose of the Study:

  • To review barrier defects observed in inflammatory bowel disease (IBD).
  • To elucidate the mechanisms by which proinflammatory cytokines modulate AJC structure and epithelial barrier function in IBD.

Main Methods:

  • This review synthesizes findings from in vitro studies and existing literature.
  • Focuses on the role of cytokines like IFN-gamma and TNF-alpha in altering AJC protein localization and function.

Main Results:

  • Proinflammatory cytokines (IFN-gamma, TNF-alpha) can induce a leaky intestinal barrier in vitro.
  • Increased intestinal permeability and altered AJC structure in IBD are associated with the internalization of junctional proteins.
  • Cytokine-mediated modulation of AJC structure directly impacts epithelial barrier integrity.

Conclusions:

  • Cytokine-induced internalization of junctional proteins is a key mechanism underlying barrier defects in IBD.
  • Understanding these mechanisms is crucial for developing therapeutic strategies targeting intestinal barrier function in IBD.