上睑下垂
骨髓
发病机制
间质细胞
细胞生物学
双歧杆菌
生物
失调
CD11c公司
肠道菌群
微生物学
化学
炎症
细胞外
免疫学
基因敲除
医学
间充质干细胞
干细胞
癌症研究
骨重建
牙周炎
益生菌
调节器
基因表达
细胞外小泡
作者
Li-Min Lei,Xiao Lin,Feng Xu,Fu‐Xing‐Zi Li,Su‐Kang Shan,Ming-Hui Zheng,Bei Guo,Ye-Chi Cao,Zhi-Ang Zhou,Si-Yang He,Yanlin Wu,X C Chen,F Zhang,Wei Zhang,J X Zhu,Yue Wang,Qi-Rong Deng,Z Y He,Feng Wu,Ling‐Qing Yuan
标识
DOI:10.1186/s12951-026-04719-1
摘要
Recent studies suggest that cold temperature (CT) exposure contributes to osteoporosis. While the gut microbiota (GM) is a key regulator of host physiology, CT conditions significantly alter its composition. In this study, we found that co-housing with room temperature (RT) mice, as well as colonization with RT-donor GM, conferred protection against CT-induced bone loss. Using 16 S rRNA gene sequencing, we demonstrated that the CT-triggered decline in intestinal Bifidobacterium pseudolongum (B. p) abundance was rescued by co-housing with RT mice. Furthermore, oral administration of B. p effectively alleviated CT-induced bone loss. Mechanistically, we identified that small extracellular vesicles derived from Bifidobacterium. pseudolongum (B. p-sEVs) were taken up by bone tissue, where they enhanced osteogenesis and suppressed pyroptosis in bone marrow stromal cells (BMSCs). Collectively, our findings suggest that the GM helps preserve bone mass via bacterial sEVs, and that the reduction of B. p and its derived sEVs drives CT-induced bone loss.
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