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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...
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Inflammatory Bowel Disease I: Ulcerative Colitis01:27

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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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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. 

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Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice
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HVEM signalling promotes colitis.

Corinne Schaer1, Stefanie Hiltbrunner, Bettina Ernst

  • 1Molecular Biomedicine, Institute of Integrative Biology, Swiss Federal Institute of Technology, Zurich, Switzerland.

Plos One
|May 3, 2011
PubMed
Summary
This summary is machine-generated.

Tumor necrosis factor super family (TNFSF) member HVEM promotes inflammatory bowel disease (IBD). Mice lacking HVEM showed reduced colitis, indicating HVEM is a potential therapeutic target for IBD.

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DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
09:04

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat

Published on: February 27, 2014

Area of Science:

  • Immunology
  • Molecular Biology
  • Gastroenterology

Background:

  • Members of the Tumor Necrosis Factor Super Family (TNFSF) are vital for cell regulation and immune homeostasis.
  • Several TNFSF members are linked to inflammatory bowel disease (IBD), presenting therapeutic opportunities.

Purpose of the Study:

  • To investigate the role of the TNFSF member HVEM in experimental models of IBD.
  • To determine if HVEM influences the development of colitis.

Main Methods:

  • Utilized mice deficient in HVEM in two distinct experimental models of IBD.
  • Induced colitis chemically (innate immunity) and via T cell transfer (adaptive immunity).

Main Results:

  • Absence of HVEM significantly reduced the severity of colitis in both models.
  • Inflammatory cytokine production was notably decreased in HVEM-deficient mice.

Conclusions:

  • HVEM signaling exacerbates experimental colitis.
  • HVEM is implicated in driving colitis mediated by both innate and adaptive immune cells.