CARD3 deficiency protects against colitis through reduced epithelial cell apoptosis
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1Departments of *Gastroenterology, Key Laboratory of Hubei Province for Digestive System Disease, †Pathology, Renmin Hospital of Wuhan University, Wuhan, China; and ‡Cardiovascular Research Institute, Wuhan University, Wuhan, China.
Insights
Loss of Caspase activation and recruitment domain 3 (CARD3) protects against inflammatory bowel disease by reducing colonic epithelial cell apoptosis, enhancing barrier function, and decreasing colitis severity.
Area of Science:
- Immunology
- Gastroenterology
- Molecular Biology
Background:
- Caspase activation and recruitment domain 3 (CARD3) is a protein kinase implicated in immune and inflammatory responses.
- Its specific role in inflammatory bowel disease (IBD) warrants further investigation.
Purpose of the Study:
- To investigate the effect of CARD3 deficiency on dextran sodium sulfate (DSS)-induced colitis.
- To elucidate the mechanisms underlying CARD3's role in intestinal inflammation.
Main Methods:
- Induction of colitis in wild-type and CARD3-deficient mice using DSS.
- Analysis of colon tissues for histological changes, immune cell infiltration, and epithelial cell apoptosis.
Main Results:
- CARD3-deficient mice exhibited reduced susceptibility to colitis, evidenced by less weight loss, lower disease activity, and improved colon histology.
- This protection correlated with decreased epithelial cell apoptosis and enhanced intestinal barrier function.
- Elevated CARD3 levels were observed in intestinal tissues from human IBD patients.
Conclusions:
- CARD3 acts as a positive regulator of intestinal epithelial cell apoptosis in the inflamed colon.
- Genetic ablation of CARD3 confers protection against colitis by preserving epithelial barrier integrity.
- Targeting CARD3 may offer a novel therapeutic strategy for managing IBD.
Background:
Caspase activation and recruitment domain 3 (CARD3) is a 61-kDa protein kinase. Recent evidence shows the importance of CARD3 in the immune response and inflammatory diseases. To elucidate its impact on inflammatory bowel disease, we studied the effects of the loss of CARD3 in the acute dextran sodium sulfate-induced colitis.
Methods:
Colitis was induced by administration of dextran sodium sulfate to wild-type and CARD3 mice. Colon tissues were analyzed.
Results:
CARD3 mice were less susceptible to the development of colitis than wild-type controls as determined by weight loss, disease activity, colon histology, neutrophil infiltration, and cytokine expression. Reduced susceptibility of CARD3 mice to colitis was closely related to increased density of colonic epithelial cells relative to wild-type controls, which was because of decreased levels of apoptosis that resulted in enhanced epithelial barrier function. Finally, CARD3 levels were increased in intestinal tissue from patients with IBD.
Conclusions:
These results imply a role for CARD3 as a positive regulator of intestinal epithelial cell apoptosis in the inflamed colon. Genetic loss of CARD3 is protective against colitis through decreased epithelial cell apoptosis and consequent enhancement of intestinal epithelial barrier function. Thus, targeted CARD3 inhibition may represent a new therapeutic approach in IBD.
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