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Related Concept Videos

Inflammatory Bowel Disease I: Ulcerative Colitis01:27

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Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
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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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Related Experiment Video

Updated: Apr 6, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
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Galectin-3 Modulates Experimental Colitis.

Elisabeth Lippert1, Manuela Stieber-Gunckel, Nadja Dunger

  • 1Department of Internal Medicine I, University Hospital Regensburg, Regensburg, Germany.

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|July 24, 2015
PubMed
Summary
This summary is machine-generated.

Galectin-3 (gal-3) treatment reduces inflammation in mouse models of acute and chronic colitis. This suggests gal-3 has a potential role in managing intestinal inflammation.

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Area of Science:

  • Immunology
  • Gastroenterology

Background:

  • Galectin-3 (gal-3) is a newly identified fibroblast activator produced by colonic epithelial cells.
  • The role of gal-3 in inflammatory bowel disease (IBD) is largely unknown.
  • This study investigates gal-3's impact on dextran sodium sulfate (DSS)-induced colitis in mice.

Purpose of the Study:

  • To determine the effect of gal-3 on fibroblast activation in vitro.
  • To evaluate the therapeutic potential of gal-3 in a mouse model of DSS-induced colitis.
  • To assess gal-3's influence on colonic cytokine expression during colitis.

Main Methods:

  • Co-incubation of colonic fibroblasts with gal-3 and other cytokines (gal-1, TGF-β1, IFNγ, IL-4, IL-10).
  • Induction of acute and chronic colitis in mice using 3% DSS in drinking water.
  • Intraperitoneal administration of recombinant gal-3 and subsequent histological and gene expression analysis of colonic tissue.

Main Results:

  • In vitro, gal-3-induced IL-8 secretion was attenuated by IL-10 and IL-4.
  • Gal-3 treatment ameliorated acute DSS-induced colitis, evidenced by increased colon length and reduced weight loss.
  • Gal-3 significantly suppressed colonic IL-6 expression in both acute and chronic colitis models.

Conclusions:

  • Galectin-3 demonstrates significant anti-inflammatory effects in experimental colitis.
  • These findings highlight gal-3 as a potential therapeutic target for intestinal inflammation.
  • Further research is warranted to explore gal-3's role in human inflammatory bowel disease.