ArticleJournal of advanced research2026
Clostridium butyricum and its metabolites regulate macrophage polarization through miR-146a to antagonize gouty arthritis.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Mechanisms of Gut Microbiota-Derived Metabolites in Treating Hyperuricemia: Natural Products as Interventions.Molecules (Basel, Switzerland) · 2026Review
- Dietary fiber deficiency exacerbates intestinal inflammation via miR-6240-enriched gut extracellular vesicles.NPJ biofilms and microbiomes · 2026Article
- Gut microbiota dysbiosis and joint diseases: advances in the gut-joint axis.Frontiers in immunology · 2026Review
- Rewiring macrophage immunometabolism in gouty arthritis: from metabolic checkpoints to intelligent nano-delivery.Frontiers in pharmacology · 2026Review
- Article
- Recent advances in the positive role ofFrontiers in immunology · 2026Review
- Microbiota-driven epigenetic programming of local immunity.Frontiers in immunology · 2026Review
- The role ofFrontiers in immunology · 2026Review
- Characterization of microbiota dysbiosis in papillary thyroid carcinoma and benign thyroid nodules: low abundance of intestinal butyrate-producing bacteria.BMC microbiology · 2025Article
- Mechanistic insights into non-coding RNAs regulate autophagy in chondrocytes and their contribution to osteoarthritis.Frontiers in medicine · 2025Review
- A systems immunology perspective on gout pathogenesis and its precision-targeted treatment strategies.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionGut microbiota modulation has recently been identified as a prospective avenue for the exploration of novel therapeutic strategies for the management of gout. Nevertheless, the application of a single specific strain or bacterial metabolite for gout intervention has rarely been explored and the underlying regulatory mechanism remains elusive.
objectivesTo ascertain the potential role and the molecular mechanism of Clostridium butyricum and butyrate in the management of gouty arthritis.
methodsA Uox-KO mouse model of gouty arthritis was developed and the composition of the gut microbiota was analyzed. C. butyricum and butyrate were supplemented to assess functional recovery and intestinal homeostasis. NanoString analysis identified miRNA variations. GC/MS measured butyric acid levels and qPCR detected the abundance of butyrate-producing enzymes and bacteria. Flow cytometry analyzed macrophage polarization and ELISA measured pro-inflammatory cytokine production. Agomir and antagomir were transfected and dual-luciferase reporter assay was adapted for validation of miRNA target binding. siRNA and rescue experiments were performed to validate the role of SOCS7 in macrophage polarization. In addition, a cohort of patients with gouty arthritis were assembled for the purpose of validating the molecular mechanism.
resultsThe results of our study demonstrated that a reduction of butyrate levels, resulting from a deficiency of butyrate-producing bacteria, leads to aberrant miR-146a expression. This, in turn, induces an imbalance in macrophage polarization and the onset of gouty arthritis. The administration of C. butyricum and butyrate demonstrated considerable anti-inflammatory efficacy by restoring intestinal homeostasis, modulating miR-146a expression, and skewing macrophage polarization. The SOCS7/JAK2-STAT3 signaling pathway was identified as a pivotal mediator in the skewing of macrophage polarization induced by miR-146a.
conclusionOur findings enrich the understanding of the regulatory mechanisms underlying macrophage polarization in gouty arthritis and highlight the potential applications of probiotics and their metabolites in clinical gout treatment.
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