ArticleFrontiers in immunology2025
miR-223 alleviates DSS-induced colitis by prompting macrophage M2 polarization through PPAR-γ/FOXO1 signaling.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- [Prediction andZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Article
- Cyclodextrins as Modulators of Regulated Cell Death: Implications for Immunometabolism and Therapeutic Innovation.Pharmaceutics · 2026Review
- Macrophages in Ulcerative Colitis: Immunomodulatory Roles, Phenotypic Switching, and Therapeutic Targeting.Journal of innate immunity · 2026Review
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Authors and funding
6 authors.
Funding
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Abstract
Background: Macrophage polarization represents a promising therapeutic target for inflammatory bowel disease (IBD). This study investigates the role of miRNA-223 (miR-223) in dextran sodium sulfate (DSS)-induced colitis and its regulation of macrophage polarization. Methods: Male C57BL/6 mice were assigned to four groups: Wild-type (WT) control, DSS-treated group (DSS), DSS+miR-223 agomir (DSS+A), and DSS+ miR-223 agomir negative control (DSS+NC). Colitis was induced with 2.5% DSS for 7 days; miR-223 agomir or NC was administered intraperitoneally on days 2-4. We evaluated disease activity index (DAI), colonic inflammation, and the expression of inflammatory mediators, peroxisome proliferator-activated receptor gamma (PPAR-γ) and forkhead box transcription factor O1 (FOXO1). Results: Histopathological analysis showed that miR-223 agomir significantly attenuated DSS-induced colon damage. Proinflammatory cytokines (TNF-α, IL-1β, IL-6) increased in DSS mice, while anti-inflammatory IL-10 decreased-trends reversed by miR-223 supplementation at mRNA/protein levels. Mechanistically, DSS elevated M1 macrophage marker iNOS and FOXO1 but reduced M2 marker Arg-1 and PPAR-γ. miR-223 agomir suppressed M1 polarization while enhancing M2 polarization by downregulating FOXO1 and upregulating PPAR-γ. Conclusion: We identify a novel dual-regulatory mechanism wherein miR-223 ameliorates colitis by shifting macrophage polarization from M1 to M2
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