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Updated: Jun 8, 2026

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
08:37

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Published on: April 21, 2015

Glycogen synthase kinase 3-β: a master regulator of toll-like receptor-mediated chronic intestinal inflammation

Claudia Hofmann1, Nadja Dunger, Jürgen Schölmerich

  • 1Department of Internal Medicine I, Regensburg University Medical Center, Germany. claudia.hofmann@klinik.uni-regensburg.de

Inflammatory Bowel Diseases
|September 18, 2010
PubMed
Abstract

Insights

Inhibition of Glycogen synthase kinase 3-beta (GSK3-β) significantly reduced chronic intestinal inflammation and inflammatory responses. GSK3-β blockade offers a potential therapeutic strategy for inflammatory bowel disease by reducing exaggerated immune reactions.

Area of Science:

  • Immunology
  • Gastroenterology
  • Pharmacology

Background:

  • Chronic colitis involves dysregulated Toll-like receptor (TLR) signaling, promoting inflammation.
  • Glycogen synthase kinase 3-beta (GSK3-β) is implicated in excessive TLR-mediated inflammatory responses.

Purpose of the Study:

  • To investigate the role of GSK3-β activity in chronic intestinal inflammation.
  • To evaluate GSK3-β inhibition as a therapeutic strategy for colitis.

Main Methods:

  • Dextran sodium sulfate (DSS) induced chronic colitis in mice.
  • Treatment with GSK3-β inhibitors (SB216763, LiCl) or controls.
  • Histological analysis, cytokine assessment, and analysis of NF-κB and CREB activity in immune cells.

Main Results:

  • GSK3-β blockade significantly reduced chronic intestinal inflammation.
  • Inhibition of GSK3-β diminished the pro-inflammatory phenotype of intestinal immune cells.
  • In vivo GSK3-β blockade shifted immune cell activity from NF-κB towards CREB.

Conclusions:

  • GSK3-β blockade attenuates excessive pro-inflammatory TLR-mediated immune responses.
  • GSK3-β inhibition is a potential therapeutic approach for inflammatory bowel disease.
  • Targeting GSK3-β may selectively reduce exaggerated immune reactions to gut microbiota.

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