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Related Experiment Video

Updated: May 20, 2026

Murine Colitis Modeling using Dextran Sulfate Sodium DSS

Murine Colitis Modeling using Dextran Sulfate Sodium DSS

Published on: January 19, 2010

Taurodeoxycholate ameliorates DSS-induced colitis in mice.

Yunyun Zou¹, Aziz Ghaderpour¹, Bolormaa Munkhbileg²

¹Wide River Institute of Immunology, Seoul National University, Hongcheon, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea.

International Immunopharmacology

|July 16, 2023

Summary

Taurodeoxycholate (TDCA) effectively treated colitis in mice by inhibiting inflammasome activation. This novel therapeutic approach targets key inflammatory pathways, offering a potential new treatment for inflammatory bowel disease (IBD).

Keywords:

GPCR19 NLRP3 P2X7R TDCA Ulcerative colitis

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Area of Science:

Gastroenterology
Immunology
Pharmacology

Background:

Inflammatory bowel disease (IBD) management often involves medications with limited efficacy or significant side effects for some patients.
Existing treatments include 5-aminosalicylic acid (5-ASA), glucocorticoids, and biologic therapies targeting TNFα, IL-12, or IL-23.
The inflammasome pathway is implicated in IBD pathogenesis, suggesting inflammasome inhibition as a therapeutic strategy.

Purpose of the Study:

To investigate the therapeutic potential of taurodeoxycholate (TDCA), a G-protein coupled receptor 19 (GPCR19) agonist, in a mouse model of colitis.
To elucidate the molecular mechanisms by which TDCA exerts its anti-inflammatory effects in the context of IBD.

Main Methods:

A dextran sodium sulfate (DSS)-induced mouse colitis model was used to assess TDCA efficacy.
In vitro studies utilized bone marrow-derived macrophages (BMDMs) to investigate TDCA's effects on inflammatory signaling pathways.
Key pathways examined included NF-κB activation, purinergic receptor P2X7 (P2X7R) signaling, NLRP3 inflammasome activation, and macrophage polarization.

Main Results:

TDCA administration significantly ameliorated DSS-induced colitis, preventing weight loss, colon shortening, and mucosal ulceration.
TDCA inhibited pro-inflammatory cytokine production and reduced the infiltration of inflammatory cells in the colon.
In vitro, TDCA suppressed NF-κB activation, downregulated P2X7R expression, inhibited ATP-induced calcium mobilization, and blocked NLRP3 inflammasome assembly and caspase-1/IL-1β maturation.

Conclusions:

TDCA demonstrates significant therapeutic efficacy in a mouse model of colitis.
TDCA acts by inhibiting both the priming and activation phases of the NLRP3 inflammasome pathway.
The findings suggest TDCA is a promising candidate for novel IBD therapies targeting inflammasome signaling.