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Murine Colitis Modeling using Dextran Sulfate Sodium DSS
Published on: January 19, 2010
Deficiency of miRNA-149-3p shaped gut microbiota and enhanced dextran sulfate sodium-induced colitis
Qingqing Feng1, Yuanqiang Li1, Hongli Zhang1
1State Key Laboratory of Chemical Resource Engineering, College of Life Science and Technology, Beijing University of Chemical Technology, Beijing, P. R. China.
Abstract:
Genetic predisposition and disruption of host gut microbiota and immune system can result in inflammatory bowel disease (IBD). Here, we show that miRNA-149-5p (miR-149-5p) and miRNA-149-3p (miR-149-3p) play crucial roles in IBD. Mice lacking miR-149-3p were considerably more susceptible to dextran sulfate sodium (DSS)-induced colitis than wild-type (WT) mice, accompanied by more serious inflammatory symptoms and increased gene expression of certain inflammatory cytokines. Both miR-149-5p and miR-149-3p suppressed colon inflammatory response in vitro and in vivo. Furthermore, we found significant differences in the composition of the gut microbiota between WT and miR-149-3p-/- mice by 16S rRNA sequencing. Co-housing endowed susceptibility to WT mice against DSS-induced colitis compared with the WT control group. However, susceptibility of miR-149-3p-/- mice against DSS-induced colitis was still present after antibiotic treatment. These findings suggest that the deletion of miR-149-3p altered gut microbiota and influenced pathogenesis of intestinal inflammation, but sensitivity of miR-149-3p-/- mice to DSS-induced colitis is not conferred by microbiota. In addition, we identified the roles of miR-149-5p and miR-149-3p in colon inflammation, which may serve as an attractive therapeutic tool for colitis or IBD, and even colitis-associated carcinoma.
Insights
MicroRNAs miR-149-5p and miR-149-3p are crucial in inflammatory bowel disease (IBD). While miR-149-3p deletion impacts gut microbiota, it does not confer colitis susceptibility, suggesting other mechanisms are involved.
Area of Science:
- Molecular Biology
- Immunology
- Microbiology
Background:
- Inflammatory bowel disease (IBD) arises from genetic factors, gut microbiota, and immune system dysregulation.
- MicroRNAs (miRNAs) are key regulators of cellular processes, including inflammation.
Purpose of the Study:
- To investigate the role of miR-149-5p and miR-149-3p in the pathogenesis of inflammatory bowel disease (IBD).
- To explore the relationship between miR-149-3p, gut microbiota, and susceptibility to dextran sulfate sodium (DSS)-induced colitis.
Main Methods:
- Utilized mouse models lacking miR-149-3p and wild-type (WT) controls.
- Induced colitis using dextran sulfate sodium (DSS).
- Analyzed inflammatory markers, gene expression, and gut microbiota composition via 16S rRNA sequencing.
Main Results:
- Mice lacking miR-149-3p exhibited increased susceptibility to DSS-induced colitis with heightened inflammation.
- Both miR-149-5p and miR-149-3p demonstrated suppressive effects on colon inflammation in vitro and in vivo.
- While miR-149-3p deletion altered gut microbiota, antibiotic treatment did not eliminate colitis susceptibility in knockout mice, indicating microbiota is not the sole driver.
Conclusions:
- miR-149-5p and miR-149-3p play significant roles in regulating colon inflammation and IBD pathogenesis.
- The absence of miR-149-3p influences gut microbiota but does not solely confer susceptibility to DSS-induced colitis.
- These miRNAs represent potential therapeutic targets for colitis, IBD, and associated cancers.
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