Related Experiment Video
Updated: Feb 10, 2026
08:39
Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
51.0K
NLRP12 Deficiency Enhances Tofacitinib Efficacy in DSS Colitis Via STAT1-M1 Polarization
Yun Yi1,2, Qiaofang Wei1,2, Siyu Chen1,2
1Department of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Inflammation
|February 8, 2026
Summary
NLRP12 deficiency enhances macrophage inflammation, increasing sensitivity to tofacitinib (JAK inhibitor) for ulcerative colitis treatment. This suggests NLRP12 and M1/M2 macrophage ratio may guide therapy.
Area of Science:
- Immunology
- Gastroenterology
- Pharmacology
Background:
- Ulcerative colitis (UC) treatment with tofacitinib (JAK inhibitor) shows limited response rates.
- NLRP12 negatively regulates inflammation and influences host-microbiota interactions.
- Macrophage polarization is critical in inflammatory responses.
Purpose of the Study:
- To investigate the role of NLRP12 in macrophage polarization and its impact on tofacitinib responsiveness in colitis.
- To determine if NLRP12 deficiency enhances JAK-STAT signaling and M1 macrophage polarization.
Main Methods:
- Induction of acute colitis in wild-type and Nlrp12 knockout mice using Dextran Sodium Sulfate (DSS).
- Administration of tofacitinib and assessment of disease severity.
- Flow cytometry analysis of macrophage infiltration and polarization (M1/M2).
- Western blot analysis of STAT1 activation in colon tissue and bone marrow-derived macrophages.
Main Results:
- Nlrp12 knockout mice showed exacerbated DSS colitis with increased M1 macrophages and elevated p-STAT1.
- Tofacitinib treatment improved colitis in both genotypes but was more effective in Nlrp12 knockout mice.
- Tofacitinib reduced M1 macrophage polarization and STAT1 activation in Nlrp12 deficient macrophages.
Conclusions:
- NLRP12 deficiency promotes M1 macrophage polarization and JAK-STAT activation, enhancing sensitivity to tofacitinib in colitis.
- Elevated M1/M2 ratio and p-STAT1 levels may serve as potential biomarkers for guiding JAK inhibitor therapy in UC.
- Targeting NLRP12 or modulating macrophage polarization could optimize treatment outcomes for ulcerative colitis.
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