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Updated: Jul 20, 2026
08:39
Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
49.9K
FGF20 modulates gut microbiota to mitigate dextran sodium sulfate-induced ulcerative colitis in mouse models
Zhongqian Jin1, Zhaoyang Liu2, Jiaxuan Pan2
1The Third Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China; School of Pharmacy, Wenzhou Medical University, Wenzhou, Zhejiang, China.
International Immunopharmacology
|September 1, 2024
Summary
Fibroblast growth factor 20 (FGF20) alleviates ulcerative colitis (UC) symptoms by improving gut microbiota balance. FGF20 therapy shows promise for treating this inflammatory bowel disease (IBD).
Area of Science:
- Gastroenterology
- Immunology
- Microbiology
Background:
- Ulcerative colitis (UC) is a major form of inflammatory bowel disease (IBD) with limited treatment options.
- The precise mechanisms underlying UC pathogenesis and potential therapeutic targets remain under investigation.
- Fibroblast growth factor 20 (FGF20) is emerging as a potential factor in UC, but its role is not fully understood.
Purpose of the Study:
- To investigate the role of FGF20 in a dextran sodium sulfate (DSS)-induced mouse model of ulcerative colitis (UC).
- To explore the therapeutic potential of FGF20 in alleviating UC symptoms and its underlying mechanisms, including effects on gut microbiota.
Main Methods:
- Established a mouse model of UC using DSS administration.
- Assessed FGF20 expression levels in serum and colonic tissues.
- Utilized FGF20 knockout and adeno-associated virus (AAV)-mediated FGF20 overexpression.
- Evaluated histological changes, inflammation markers, and expression of tight junction and mucin proteins.
- Analyzed gut microbiota composition and performed microbiota depletion and transplantation experiments.
Main Results:
- DSS-induced UC mice exhibited reduced FGF20 expression.
- FGF20 overexpression significantly ameliorated UC symptoms, including reduced inflammation, improved tissue integrity, and restored goblet cell density.
- FGF20 treatment reversed DSS-induced gut dysbiosis, promoting beneficial bacteria and reducing harmful ones.
- The therapeutic effects of FGF20 were dependent on the presence of gut microbiota, as evidenced by antibiotic treatment and fecal microbiota transplantation.
Conclusions:
- FGF20 plays a protective role in experimental ulcerative colitis.
- FGF20 exerts therapeutic benefits in UC, at least partially, through modulation of the gut microbiota.
- FGF20 represents a potential therapeutic agent for UC, with its efficacy linked to gut microbial interactions.
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