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儿童肠道微生物群来源的细胞外囊泡进入骨骼以维持骨量和强度。

Extracellular Vesicles from Child Gut Microbiota Enter into Bone to Preserve Bone Mass and Strength.

机构信息

Department of Orthopedics Xiangya Hospital Central South University Changsha Hunan 410008 China.

Movement System Injury and Repair Research Center Xiangya Hospital Central South University Changsha Hunan 410008 China.

出版信息

Adv Sci (Weinh). 2021 Feb 17;8(9):2004831. doi: 10.1002/advs.202004831. eCollection 2021 May.

DOI:10.1002/advs.202004831
PMID:33977075
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8097336/
Abstract

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 (). Direct replenishment of 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 -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 mediates the CGM-induced anti-osteoporotic effects and presents a novel mechanism underlying the exchange of signals between GM and host bone.

摘要

最近,肠道微生物群(GM)被证明是骨稳态的调节剂,而 GM 调节骨量的机制仍在研究中。在这里,人们发现来自儿童的 GM(CGM)定植而不是来自老年人的 GM(EGM)可防止常规饲养、卵巢切除(OVX)诱导的骨质疏松症小鼠的骨量和骨强度下降。16S rRNA 基因测序显示,CGM 逆转了 OVX 诱导的 () 减少。直接补充 足以纠正 OVX 诱导的骨代谢失衡并预防骨质疏松症。机制研究表明,细胞外囊泡(EVs)的分泌对于 CGM-和 -诱导的骨保护作用是必需的,这些纳米囊泡可以进入并积累到骨组织中,通过增强成骨活性和抑制破骨细胞形成来减轻 OVX 诱导的骨质疏松表型。该研究确定了肠道细菌 介导了 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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/191a/8097336/d1f5bbe7d12f/ADVS-8-2004831-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/191a/8097336/06b3d4113caf/ADVS-8-2004831-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/191a/8097336/a42ea9a11fd0/ADVS-8-2004831-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/191a/8097336/71d45a747c09/ADVS-8-2004831-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/191a/8097336/d64d76b88783/ADVS-8-2004831-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/191a/8097336/d1f5bbe7d12f/ADVS-8-2004831-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/191a/8097336/06b3d4113caf/ADVS-8-2004831-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/191a/8097336/e50057ac74ed/ADVS-8-2004831-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/191a/8097336/a42ea9a11fd0/ADVS-8-2004831-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/191a/8097336/71d45a747c09/ADVS-8-2004831-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/191a/8097336/d64d76b88783/ADVS-8-2004831-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/191a/8097336/d1f5bbe7d12f/ADVS-8-2004831-g002.jpg

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