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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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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 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 I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

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Peptic Ulcer Disease II: Pathophysiology01:24

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Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
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Decrease of peripheral and intestinal NKG2A-positive T cells in patients with ulcerative colitis.

Takehiko Katsurada1, Waka Kobayashi, Utano Tomaru

  • 1Department of Pathology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.

Plos One
|September 13, 2012
PubMed
Summary

Inhibitory natural killer receptors (iNKRs) like NKG2A are crucial in inflammatory bowel disease (IBD). Reduced NKG2A+ T cells in the gut may drive ulcerative colitis pathogenesis.

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Published on: May 21, 2012

Area of Science:

  • Immunology
  • Gastroenterology
  • Cell Biology

Background:

  • Inflammatory bowel disease (IBD) encompasses Crohn's disease (CD) and ulcerative colitis (UC).
  • Inhibitory natural killer receptors (iNKRs) regulate immune cell activity.
  • The role of NKG2A, an iNKR, in T cells during IBD is not fully understood.

Purpose of the Study:

  • To investigate the function of NKG2A+ T cells in a mouse model of colitis and in human IBD patients.
  • To determine if NKG2A expression on T cells correlates with IBD development or severity.

Main Methods:

  • Analysis of NKG2A expression on T cells in a dextran sulfate sodium (DSS)-induced mouse colitis model.
  • Flow cytometry to quantify NKG2A+ T cells in peripheral blood and intestinal tissue.
  • Comparison of NKG2A+ T cell frequencies in peripheral blood and intestinal tissue of UC patients, CD patients, and healthy controls.

Main Results:

  • In DSS-induced colitis, NKG2A+ T cells decreased in peripheral blood but increased in the intestine, indicating migration to inflamed sites.
  • Blocking NKG2A exacerbated colitis in the mouse model.
  • UC patients showed significantly lower frequencies of peripheral blood NKG2A+ T cells compared to CD patients and healthy controls.
  • Intestinal T cells from UC patients also had reduced NKG2A+ cell frequencies, contrasting with the mouse model.

Conclusions:

  • NKG2A+ T cells are mobilized to inflamed tissues during experimental colitis.
  • Inadequate infiltration of NKG2A+ T cells into the intestine may contribute to the pathogenesis of ulcerative colitis.
  • NKG2A+ T cell frequency in peripheral blood could serve as a biomarker for UC.