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Updated: Apr 8, 2026
Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
Disrupting endogenous retroelements with a reverse transcriptase inhibitor alleviates DSS-induced colitis in mice
Yifan Niu1, Yu Liu1, Xiang Ma1
1College of Animal Science and Technology ＆ College of Veterinary Medicine, Zhejiang A＆F University, Key Laboratory of Applied Technology on Green-Eco-Healthy Animal Husbandry of Zhejiang Province, Provincial Engineering Research Center for Animal Health Diagnostics ＆ Advanced Technology, Zhejiang International Science and Technology Cooperation Base for Veterinary Medicine and Health Management, China Australia Joint Laboratory for Animal Health Big Data Analytics, Hangzhou, Zhejiang 311300, China.
Azidothymidine (AZT), an endogenous retroelement inhibitor, alleviates colitis by blocking M1 macrophage polarization. This study suggests targeting retroelements offers a novel therapeutic strategy for colitis treatment.
Area of Science:
- Immunology
- Gastroenterology
- Molecular Biology
Background:
- Endogenous retroelements are crucial for immune homeostasis but their activation can promote inflammation.
- M1 macrophages, induced by pro-inflammatory cytokines, contribute to colitis development.
- The cGAS/STING pathway is implicated in inflammatory responses triggered by retroelement activation.
Purpose of the Study:
- To investigate if Azidothymidine (AZT), a reverse transcriptase inhibitor, can mitigate colitis.
- To determine if AZT influences M1 macrophage polarization by inhibiting endogenous retroelements.
- To explore AZT's potential therapeutic role in colitis via modulating the cGAS/STING pathway.
Main Methods:
- Utilized a dextran sodium sulfate (DSS)-induced colitis mouse model and lipopolysaccharide (LPS)-stimulated RAW264.7 cells.
- Assessed endogenous retroelement expression in colonic tissues and M1 macrophages.
- Evaluated the impact of AZT on the cGAS/STING/NF-κB pathway and pro-inflammatory cytokine levels.
Main Results:
- Upregulated endogenous retroelements were observed in colitis models; AZT treatment significantly reduced their expression.
- AZT administration led to downregulation of the cGAS/STING/NF-κB pathway and associated pro-inflammatory cytokines.
- AZT treatment significantly alleviated symptoms in the DSS-induced colitis mouse model.
Conclusions:
- AZT effectively rescues DSS-induced colitis, likely by inhibiting M1 macrophage polarization through the cGAS/STING/NF-κB pathway.
- Pharmacological inhibition of endogenous retroelements presents a promising new therapeutic avenue for colitis.
- AZT demonstrates potential as a treatment for inflammatory conditions driven by retroelement activation.
