Related Experiment Video
Updated: Feb 18, 2026

An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
Published on: December 3, 2020
The Proton-activated Receptor GPR4 Modulates Intestinal Inflammation
Yu Wang1,2, Cheryl de Vallière1, Pedro H Imenez Silva2
1Department of Gastroenterology and Hepatology, University Hospital Zurich, Zurich, Switzerland.
Absence of GPR4 ameliorates colitis in animal models of inflammatory bowel disease [IBD]. This suggests GPR4 plays a key role in mucosal inflammation and could be a therapeutic target for IBD treatment.
Area of Science:
- Gastroenterology and Immunology
- Molecular and Cellular Biology
Background:
- Intraluminal intestinal pH decreases during active inflammation in inflammatory bowel disease [IBD].
- Proton-sensing G-protein coupled receptors, including GPR4, are recently identified.
- The role of GPR4 in intestinal inflammation remains to be elucidated.
Purpose of the Study:
- To investigate the involvement of GPR4 in intestinal inflammation.
- To assess the therapeutic potential of targeting GPR4 in IBD models.
Main Methods:
- Murine colitis models were used, including dextran sulphate sodium [DSS] administration and IL-10 deficient mice.
- Colitis severity was evaluated by body weight, colonoscopy, histology, cytokine mRNA expression, and myeloperoxidase [MPO] activity.
- Rectal prolapse incidence and lamina propria leukocytes [LPLs] were analyzed in spontaneous colitis models.
Main Results:
- Gpr4-/- mice exhibited reduced severity in DSS-induced colitis.
- Absence of GPR4 delayed and mitigated rectal prolapse in IL-10 deficient mice.
- Gpr4-/-/Il-10-/- mice showed decreased inflammatory markers, immune cell infiltration, and cytokine expression.
Conclusions:
- GPR4 deficiency ameliorates colitis in experimental models.
- GPR4 plays a significant regulatory role in mucosal inflammation.
- Therapeutic inhibition of GPR4 may offer a novel treatment strategy for IBD.
More Related Videos
08:37Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
09:31Effects of Taste Signaling Protein Abolishment on Gut Inflammation in an Inflammatory Bowel Disease Mouse Model
Published on: November 9, 2018
Related Concept Videos
Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists
GPCRs Regulate Adenylyl Cylase Activity
G-Protein Gated Ion Channels
Sensory...
Renewal of Intestinal Stem Cells
Inflammatory Bowel Disease IV: Pharmacological Management
Pharmacologic...
Regulation of the Digestive System
The effectors in this regulation system are glands and smooth muscles. Activation of...