ArticleScientific reports2024
Propionibacterium freudenreichii MJ2-derived extracellular vesicles inhibit RANKL-induced osteoclastogenesis and improve collagen-induced rheumatoid arthritis.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The crosstalk network of non-coding RNAs: Emerging opportunities for the clinical application of osteoporosis.Non-coding RNA research · 2026Review
- Extracellular vesicles in rheumatoid arthritis: emerging roles in progression, diagnosis, and therapeutic development.Frontiers in immunology · 2026Review
- Mammalian, plant, and gut microbiota-derived extracellular vesicles as emerging therapeutics for bone diseases.Frontiers in bioengineering and biotechnology · 2026Review
- Dairy Propionibacteria: Probiotic Properties and Their Molecular Bases.Biomolecules · 2025Review
- Probiotic-derived extracellular vesicles: the next breakthrough in postbiotics for rheumatoid arthritis.Frontiers in immunology · 2025Review
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Authors and funding
3 authors.
Funding
Abstract
Rheumatoid arthritis causes excessive bone loss by stimulating osteoclast differentiation. Extracellular vesicles are valuable disease markers, conveyors of distant cell-to-cell communication, and carriers for drug delivery. The aim of this study was to investigate the anti-osteoclastogenic effects of extracellular vesicles derived from dairy Propionibacterium freudenreichii MJ2 (PFEVs) and the improvement effect of PFEVs on collagen-induced arthritis (CIA) animal model. PFEVs were observed by scanning electron microscopy, transmission electron microscopy, nanoparticle tracking analysis, and LC-MS/MS. The inhibitory activity of PFEVs against receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclast differentiation was investigated in RAW 264.7 cells. PFEVs significantly decreased the expression levels of genes and proteins related to osteoclast differentiation. PFEVs decreased RANK-RANKL binding. In a CIA mouse model, PFEVs treatment significantly reduced arthritis scores and collagen-specific immunoglobulins. PFEVs treatment also reduced pro-inflammatory cytokines and increased anti-inflammatory cytokines. The anti-inflammatory effects were confirmed by H&E staining, and PFEVs treatment inhibited osteoclastogenesis in the CIA mouse model. In conclusion, PFEVs inhibited osteoclast differentiation by inhibiting RANK-RANKL signaling, thereby decreasing the expression of osteoclast differentiation-related genes. PFEVs also improved collagen-induced arthritis by inhibiting inflammation and osteoclastogenesis.
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