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<p>Endometriosis (EMS) remains understudied in effective management strategies. The interplay between macrophage dysfunction and microbiota-derived immune signals emerges as a potential mechanism in EMS pathogenesis, suggesting its relevance for future therapeutic exploration. In this study, we established mouse models to demonstrate that gut microbiota modulated EMS development. Integrated microbial and metabolomic profiling identified <i>Parabacteroides goldsteinii</i> (Pg) as a promising probiotic candidate, whose downstream metabolite 7-ketolithocholic acid (7-KLCA) exhibiting therapeutic efficacy in ameliorating EMS phenotypes upon supplementation. Mechanistically, Pg reshapes its bile acid (BA) metabolism to elevate 7-KLCA. This bioactive metabolite acts via the receptor TGR5 to suppress PPARγ expression and activate GPR132, thereby enhancing efferocytosis and promoting M1 macrophage polarization. These findings uncover a gut-metabolite-immune regulatory axis through which Pg reprograms macrophage function to restrain EMS progression, offering a potential microbial perspective for this chronic condition.</p>

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Parabacteroides goldsteinii and its metabolite 7-KLCA attenuate endometriosis via TGR5 to reprogram macrophages by modulating the PPARγ/GPR132 axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月22日

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  • Yun Chen,
  • Yuqing Qiu,
  • Feifei Pan,
  • Yanqin Zheng,
  • Jingyao Wang,
  • Kunxiang Gong,
  • Lirong Guo,
  • Yiming Song,
  • Zixin Tao,
  • Kun Shi

摘要

Endometriosis (EMS) remains understudied in effective management strategies. The interplay between macrophage dysfunction and microbiota-derived immune signals emerges as a potential mechanism in EMS pathogenesis, suggesting its relevance for future therapeutic exploration. In this study, we established mouse models to demonstrate that gut microbiota modulated EMS development. Integrated microbial and metabolomic profiling identified Parabacteroides goldsteinii (Pg) as a promising probiotic candidate, whose downstream metabolite 7-ketolithocholic acid (7-KLCA) exhibiting therapeutic efficacy in ameliorating EMS phenotypes upon supplementation. Mechanistically, Pg reshapes its bile acid (BA) metabolism to elevate 7-KLCA. This bioactive metabolite acts via the receptor TGR5 to suppress PPARγ expression and activate GPR132, thereby enhancing efferocytosis and promoting M1 macrophage polarization. These findings uncover a gut-metabolite-immune regulatory axis through which Pg reprograms macrophage function to restrain EMS progression, offering a potential microbial perspective for this chronic condition.