Gut commensal Olsenella profusa promotes endometriosis via lysophosphatidylcholine metabolite

Yuying Chen, Chen Y, Ziwei Zhou, Zhou Z, Biqi Huang, Huang B, Xie X, Xunjie Xie, Cao Y, Yuzhen Cao, Zeng S, Shanshui Zeng, Bingyu Li, Li B, Xia F, Fangbo Xia, Peng L, Li Peng, Jiarui Liang, Liang J, Chen S, Shulei Chen, Liu H, Haojing Liu, Zhou H, Hongwei Zhou, Ma Y, Ying Ma, Zhang D, Dongxin Zhang
Cell reports. Medicine · 2026 · pp. 102970 · doi:10.1016/j.xcrm.2026.102970 · PMID:42556341 · W7172538603
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The gut bacterium *Olsenella profusa* promotes endometriosis progression by producing lysophosphatidylcholine (16:0), which enhances endometrial stromal cell proliferation and migration.

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Abstract

Endometriosis (EM) is an intractable gynecological condition with uncertain etiology. Gut microbiota have been increasingly implicated in EM, yet the underlying mechanisms remain unclear. Here, we identify a gut microbe-metabolite-uterus axis that drives EM pathogenesis. In our EM cohort, we found that the gut bacterium Olsenella profusa (O. profusa) and metabolite lysophosphatidylcholine (LPC) (16:0) were significantly enriched in patients with EM and showed positive correlation. In a mouse model of EM, oral gavage with O. profusa accelerated ectopic lesion growth through producing LPC (16:0) via its phospholipase, an effect recapitulated by LPC (16:0) alone. Mechanistically, LPC (16:0) promotes EM by inducing endometrial stromal cell proliferation and migration through the secreted phosphoprotein 1 (SPP1)-PI3K-AKT pathway. Moreover, O. profusa and LPC (16:0) show potential as early diagnostic biomarkers. This study suggests a causal role for the gut O. profusa-LPC (16:0) metabolic axis in EM progression and identifies promising targets for diagnosis and therapy.

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SciLite annotations

organisms 7
strain d315a-29 intestinal metagenome microbiota intestinal metagenome candidatus gribaldobacteria bacterium strain d315a-29 transgenic mice
chemicals 2
lysophosphatidylcholine lysophosphatidylcholine

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