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Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
Protein Kinase D2 Protects against Acute Colitis Induced by Dextran Sulfate Sodium in Mice
Jing Xiong1, Ming-Feng Zhou1,2, Ya-Dong Wang1
1Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Abstract:
Inflammatory bowel disease is characterized by dysregulation of the mucosal immune system resulting from impaired intestinal epithelial barrier function. Protein kinase D2 has been implicated in the regulation of immune responses. The present study was to define PKD2 might affect murine colitis. Colitis was induced in wild-type mice (PKD2WT/WT) and PKD2 catalytic activity deficient mice (PKD2SSAA/SSAA) with dextran sulfate sodium. PKD2SSAA-knockin mice displayed catalytic activity deficiency and increased susceptibility to DSS-induced colitis with enhanced weight loss, colonic inflammation compared with PKD2WT/WT mice. Furthermore, crucial inflammatory cytokines mRNA levels in PKD2SSAA-knockin mice were higher than controls accompanied with down-regulation of ZO-1, MUC2 and intestinal barrier dysfunction. However, there were no differences in the proliferation or apoptosis of intestinal epithelial cells in PKD2SSAA-knockin mice compared with wild-type controls. In addition, PKD2 expression was repressed in patients with IBD compared with healthy controls. These studies suggested that activation of PKD2 in the colonic epithelium microenvironment may contribute to protect against DSS-induced colitis through regulation of intestinal mucosal immunity and barrier function.
Insights
Protein kinase D2 (PKD2) activation protects against inflammatory bowel disease. PKD2 deficiency in mice worsened colitis, suggesting PKD2
Area of Science:
- Immunology
- Gastroenterology
- Molecular Biology
Background:
- Inflammatory bowel disease (IBD) involves immune dysregulation and impaired intestinal barrier function.
- Protein kinase D2 (PKD2) plays a role in immune response regulation.
Purpose of the Study:
- To investigate the role of Protein Kinase D2 (PKD2) in murine colitis.
- To determine if PKD2 catalytic activity influences susceptibility to dextran sulfate sodium (DSS)-induced colitis.
Main Methods:
- Induction of colitis in wild-type (PKD2WT/WT) and catalytic activity-deficient (PKD2SSAA/SSAA) mice using DSS.
- Assessment of clinical signs, colonic inflammation, cytokine mRNA levels, and intestinal barrier markers (ZO-1, MUC2).
- Comparison of intestinal epithelial cell proliferation and apoptosis between genotypes.
- Analysis of PKD2 expression in human IBD patients versus healthy controls.
Main Results:
- PKD2SSAA/SSAA mice showed increased susceptibility to DSS-induced colitis, with greater weight loss and colonic inflammation.
- PKD2SSAA/SSAA mice exhibited elevated inflammatory cytokine mRNA levels and intestinal barrier dysfunction (down-regulation of ZO-1 and MUC2).
- No significant differences in intestinal epithelial cell proliferation or apoptosis were observed between PKD2SSAA/SSAA and wild-type mice.
- PKD2 expression was found to be repressed in patients with IBD compared to healthy individuals.
Conclusions:
- Catalytic activity of PKD2 is crucial for protection against DSS-induced colitis in mice.
- PKD2 activation in the colonic epithelium may protect against colitis by modulating mucosal immunity and intestinal barrier function.
- Reduced PKD2 expression in IBD patients suggests a potential role in disease pathogenesis.
