Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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...
Drugs for Treatment of Ulcerative Colitis in IBD01:29

Drugs for Treatment of Ulcerative Colitis in IBD

Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide generation. 
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 IV: Pharmacological Management01:29

Inflammatory Bowel Disease IV: Pharmacological Management

Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...
Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents

Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel Disease...
Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Diagnostic delay in inflammatory bowel diseases in a German population.

World journal of gastroenterology·2024
Same author

Selection of cross-reactive T cells by commensal and food-derived yeasts drives cytotoxic T<sub>H</sub>1 cell responses in Crohn's disease.

Nature medicine·2023
Same author

A Notch/STAT3-driven Blimp-1/c-Maf-dependent molecular switch induces IL-10 expression in human CD4<sup>+</sup> T cells and is defective in Crohn´s disease patients.

Mucosal immunology·2022
Same author

[Position paper on endoscopic reporting in IBD].

Zeitschrift fur Gastroenterologie·2021
Same author

Level of Tumor Necrosis Factor Production by Stimulated Blood Mononuclear Cells Can Be Used to Predict Response of Patients With Inflammatory Bowel Diseases to Infliximab.

Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association·2020
Same author

Human Anti-fungal Th17 Immunity and Pathology Rely on Cross-Reactivity against Candida albicans.

Cell·2019

Related Experiment Video

Updated: Jun 2, 2026

Evaluating Therapeutic Interventions in the SHIP-deficient Mouse Model of Crohn Disease-like Ileitis and Fibrosis
09:44

Evaluating Therapeutic Interventions in the SHIP-deficient Mouse Model of Crohn Disease-like Ileitis and Fibrosis

Published on: October 14, 2025

Ulcerative colitis: immune function, tissue fibrosis and current therapeutic considerations.

Jochen Maul1, Martin Zeitz

  • 1Department of Medicine I (Gastroenterology/Rheumatology/Infectious Diseases), Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, 12200, Berlin, Germany.

Langenbeck'S Archives of Surgery
|April 12, 2011
PubMed
Summary

Ulcerative colitis (UC) involves genetic and environmental factors leading to chronic inflammation and fibrosis. Future therapies targeting specific cells and cytokines may prevent this progression.

More Related Videos

Performing Colonoscopic-Guided Pinch Biopsies in Mice and Evaluating Subsequent Tissue Changes
08:52

Performing Colonoscopic-Guided Pinch Biopsies in Mice and Evaluating Subsequent Tissue Changes

Published on: February 5, 2021

Related Experiment Videos

Last Updated: Jun 2, 2026

Evaluating Therapeutic Interventions in the SHIP-deficient Mouse Model of Crohn Disease-like Ileitis and Fibrosis
09:44

Evaluating Therapeutic Interventions in the SHIP-deficient Mouse Model of Crohn Disease-like Ileitis and Fibrosis

Published on: October 14, 2025

Performing Colonoscopic-Guided Pinch Biopsies in Mice and Evaluating Subsequent Tissue Changes
08:52

Performing Colonoscopic-Guided Pinch Biopsies in Mice and Evaluating Subsequent Tissue Changes

Published on: February 5, 2021

Area of Science:

  • Gastroenterology
  • Immunology
  • Fibrosis Research

Background:

  • Ulcerative colitis (UC) is a complex inflammatory bowel disease.
  • It results from interactions between genetic, environmental, and microbial factors.
  • Chronic inflammation in UC leads to significant tissue fibrosis.

Purpose of the Study:

  • To review current knowledge on UC pathogenesis.
  • To discuss genetic susceptibility, focusing on the IL-12/IL-23 pathway.
  • To explore pathophysiologic roles of cytokines and immune cells in UC.

Main Methods:

  • Review of existing literature on UC.
  • Analysis of genetic and cytokine involvement.
  • Discussion of immune cell contributions (T cells, epithelial cells, fibroblasts).
  • Examination of animal models in inflammatory bowel disease research.

Main Results:

  • The IL-12/IL-23 pathway is a key genetic factor in UC.
  • Specific cytokines (IL-13, IL-23, TGFβ1) and immune cells play crucial roles.
  • Fibrosis is a consequence of perpetuated inflammatory mechanisms.

Conclusions:

  • Future UC therapies will target specific cell types and signaling pathways.
  • Therapeutic strategies include blocking activation, migration, and cytokine activity.
  • Early intervention may prevent inflammation perpetuation and subsequent fibrosis.