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<p><i>Prevotella copri</i>, a predominant commensal bacterium in the human gut, exhibits positive or negative correlations with multiple metabolic disorders through its abundance dynamics. Although its association with rheumatoid arthritis pathogenesis is established, the effect of <i>P. copri</i> on bone metabolism remains elusive. This study demonstrates that <i>P. copri</i> exposure induces systemic bone metabolic imbalance in both normal physiological murine models and in vitro-cultured bone marrow-derived adherent cells (BMDCs), which is characterized by exacerbated osteoclastogenesis. Notably, succinate acts as a critical bioactive metabolite, with its specific receptor SUCNR1 being involved in its regulation on bone metabolism. <i>P. copri</i> or succinate intervention triggers bone inflammatory responses, prominently elevating IL-6 expression. Intriguingly, the osteoclastic activation is abolished in <i>Il-6</i>-knockout mice upon <i>P. copri</i> or succinate challenge. These findings delineate a ‌succinate-SUCNR1-IL-6 signaling axis‌ through which <i>P. copri</i> disrupts bone homeostasis, proposing novel therapeutic strategies for bone disorders such as osteoporosis via modulating gut microbiota composition (e.g., diet-mediated <i>Prevotella</i> suppression), reducing succinate bioavailability, and pharmacological antagonism of SUCNR1.</p>

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Prevotella copri impairs bone mass via osteoclast activation in mice

  • 期刊论文

  • 发表日期：

    2026年7月8日

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  • Rui Li,
  • Haiyan Zhang,
  • Shiyong Xin,
  • Tiantian Zeng,
  • Wenchu Qian,
  • Yawen Sun,
  • Yunfei Cao,
  • Yuxin Wang,
  • Bin Li,
  • Ming Tian,
  • Hai Lin,
  • Haifang Li

摘要

Prevotella copri, a predominant commensal bacterium in the human gut, exhibits positive or negative correlations with multiple metabolic disorders through its abundance dynamics. Although its association with rheumatoid arthritis pathogenesis is established, the effect of P. copri on bone metabolism remains elusive. This study demonstrates that P. copri exposure induces systemic bone metabolic imbalance in both normal physiological murine models and in vitro-cultured bone marrow-derived adherent cells (BMDCs), which is characterized by exacerbated osteoclastogenesis. Notably, succinate acts as a critical bioactive metabolite, with its specific receptor SUCNR1 being involved in its regulation on bone metabolism. P. copri or succinate intervention triggers bone inflammatory responses, prominently elevating IL-6 expression. Intriguingly, the osteoclastic activation is abolished in Il-6-knockout mice upon P. copri or succinate challenge. These findings delineate a ‌succinate-SUCNR1-IL-6 signaling axis‌ through which P. copri disrupts bone homeostasis, proposing novel therapeutic strategies for bone disorders such as osteoporosis via modulating gut microbiota composition (e.g., diet-mediated Prevotella suppression), reducing succinate bioavailability, and pharmacological antagonism of SUCNR1.