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Related Concept Videos

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...
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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...
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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
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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...
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Various diagnostic tests are employed in the diagnostic process for Inflammatory Bowel Disease (IBD), particularly to differentiate between Crohn's disease and ulcerative colitis.
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Inflammatory bowel disease (IBD) encompasses two major chronic disorders—ulcerative colitis and Crohn’s disease—each characterized by relapsing episodes of gastrointestinal inflammation. Although they share certain clinical features, their patterns of involvement and manifestations differ in ways that aid diagnosis and guide management.Ulcerative ColitisUlcerative colitis is limited to the colon and rectum and involves continuous inflammation of the mucosal layer. The disease course is marked...

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Chronic Salmonella Infection Induced Intestinal Fibrosis
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NF-kappaB in inflammatory bowel disease.

I Atreya1, R Atreya, M F Neurath

  • 1Institute of Molecular Medicine and I. Medical Clinic, University of Mainz, Mainz, Germany.

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Inflammatory bowel disease (IBD) involves gut mucosal immune system imbalance. Nuclear transcription factor kappaB (NF-kappaB) activation drives inflammation and tissue damage, suggesting it as a therapeutic target for IBD.

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Area of Science:

  • Immunology
  • Gastroenterology
  • Molecular Biology

Background:

  • The gut mucosal immune system maintains a balance between pro- and anti-inflammatory responses to manage pathogens and harmless antigens.
  • In inflammatory bowel disease (IBD), this balance is disrupted, favoring pro-inflammatory reactions.
  • Chronic inflammation in IBD leads to colonic tissue damage due to hyperactivated immune cells and elevated pro-inflammatory cytokines.

Purpose of the Study:

  • To review the complex role of the nuclear transcription factor kappaB (NF-kappaB) in the pathogenesis of IBD.
  • To discuss current therapeutic strategies targeting NF-kappaB activation for IBD treatment.

Main Methods:

  • Literature review focusing on the immunological mechanisms in IBD.
  • Analysis of the role of NF-kappaB in regulating pro-inflammatory gene expression.
  • Examination of pharmacological approaches to inhibit NF-kappaB.

Main Results:

  • NF-kappaB is a key regulator identified in IBD pathogenesis.
  • NF-kappaB activation is significantly increased in IBD patients.
  • NF-kappaB influences mucosal inflammation by promoting pro-inflammatory gene expression.

Conclusions:

  • NF-kappaB plays a critical role in the chronic mucosal inflammation characteristic of IBD.
  • Targeting NF-kappaB activation presents a promising therapeutic avenue for developing new IBD treatments.