Recently, the gut microbiota (GM) has been shown to be a regulator of bone homeostasis and the mechanisms by which GM modulates bone mass are still being investigated. Here, it is found that colonization with GM from children (CGM) but not from the elderly (EGM) prevents decreases in bone mass and bone strength in conventionally raised, ovariectomy (OVX)‐induced osteoporotic mice. 16S rRNA gene sequencing reveals that CGM reverses the OVX‐induced reduction of Akkermansia muciniphila (Akk). Direct replenishment of Akk is sufficient to correct the OVX‐induced imbalanced bone metabolism and protect against osteoporosis. Mechanistic studies show that the secretion of extracellular vesicles (EVs) is required for the CGM‐ and Akk‐induced bone protective effects and these nanovesicles can enter and accumulate into bone tissues to attenuate the OVX‐induced osteoporotic phenotypes by augmenting osteogenic activity and inhibiting osteoclast formation. The study identifies that gut bacterium Akk mediates the CGM‐induced anti‐osteoporotic effects and presents a novel mechanism underlying the exchange of signals between GM and host bone.

中文翻译：

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儿童肠道微生物群的细胞外囊泡进入骨骼以保持骨质和强度

最近，肠道微生物群 (GM) 已被证明是骨稳态的调节者，并且 GM 调节骨量的机制仍在研究中。在这里，我们发现，在传统饲养的卵巢切除术 (OVX) 诱导的骨质疏松小鼠中，儿童 (CGM) 而非老年人 (EGM) 的 GM 定植可以防止骨量和骨强度的下降。16S rRNA 基因测序表明，CGM 可逆转 OVX 诱导的Akkermansia muciniphila ( Akk ) 减少。直接补充Akk足以纠正OVX引起的骨代谢失衡并预防骨质疏松症。机制研究表明，CGM 和Akk诱导的骨保护作用需要细胞外囊泡 (EV) 的分泌，这些纳米囊泡可以进入并积聚到骨组织中，通过增强成骨活性和抑制破骨细胞来减轻 OVX 诱导的骨质疏松表型形成。该研究发现肠道细菌Akk介导 CGM 诱导的抗骨质疏松作用，并提出了 GM 和宿主骨之间信号交换的新机制。