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Updated: Jan 26, 2026

Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
Extracellular DNA is Increased in Dextran Sulphate Sodium-Induced Colitis in Mice.
M Maronek1, B Gromova1, R Liptak1
1Institute of Molecular Biomedicine, Faculty of Medicine, Comenius University, Bratislava, Slovak Republic.
Extracellular DNA (ecDNA) may drive inflammation in inflammatory bowel disease. Studies show higher ecDNA concentrations and lower deoxyribonuclease activity in mice with colitis, suggesting ecDNA
Area of Science:
- Gastroenterology
- Molecular Biology
- Immunology
Background:
- Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, is increasing globally.
- Current therapies for IBD are often inadequate, leading to complications and relapses.
- Extracellular DNA (ecDNA) is DNA outside of cells and is implicated in inflammatory responses.
Purpose of the Study:
- To investigate the association between colitis and extracellular DNA (ecDNA) concentration.
- To explore the role of ecDNA in the inflammatory processes of the colon.
Main Methods:
- Induction of colitis in male C57BL/6 mice using 2% dextran sulfate sodium (DSS).
- Assessment of clinical signs including weight loss, stool consistency, and colon length after 7 days.
- Quantification of ecDNA concentration and deoxyribonuclease activity in colon tissue.
Main Results:
- DSS-induced colitis resulted in significant weight loss, increased stool consistency, and shortened colons compared to controls.
- Mice with colitis exhibited higher concentrations of extracellular DNA (ecDNA) in the colon.
- Deoxyribonuclease activity was found to be lower in the colons of mice with DSS-induced colitis.
Conclusions:
- Elevated ecDNA levels correlate with colitis in a mouse model.
- Reduced deoxyribonuclease activity may contribute to increased ecDNA accumulation during colitis.
- Extracellular DNA (ecDNA) presents a potential pathogenetic factor and a biomarker for inflammatory bowel disease.
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