J Clin Invest. 2021 Mar 1;131(5). doi: 10.1172/JCI146619.
Osteoporosis is a serious clinical problem that often follows the accelerated bone loss that occurs after the estrogen withdrawal of menopause. In order to better understand the mechanism that produces estrogen withdrawal-induced bone loss, Yu and Pal et al., as reported in this issue of the JCI, examined mice that underwent ovariectomy (OVX). In C57BL/6 mice with enhanced Th17 cells in gut tissue, the authors demonstrated that OVX increased migration of TNF-expressing Th17 cells from the gut to the bone marrow. Furthermore, they found that manipulation of the pathways by which lymphocytes migrate and home to bone marrow prevented the increase of TNF+, Th17 cells in bone marrow after OVX in mice and the trabecular, but not cortical, bone loss in this model. These results argue that interactions of the gut microbiota with the immune system are involved in the effects of estrogen withdrawal on trabecular bone.
骨质疏松症是一个严重的临床问题,常发生在绝经后雌激素流失导致的骨量加速流失之后。为了更好地理解产生雌激素流失诱导的骨丢失的机制,Yu 和 Pal 等人在本期 JCI 上报道,检查了接受卵巢切除术(OVX)的小鼠。在肠道组织中 Th17 细胞增强的 C57BL/6 小鼠中,作者证明 OVX 增加了表达 TNF 的 Th17 细胞从肠道向骨髓的迁移。此外,他们发现,淋巴细胞迁移和归巢到骨髓的途径的操纵可防止 OVX 后小鼠骨髓中 TNF+、Th17 细胞的增加以及该模型中骨小梁而非皮质骨的丢失。这些结果表明,肠道微生物群与免疫系统的相互作用参与了雌激素流失对骨小梁的影响。