Gut commensal Olsenella profusa promotes endometriosis via lysophosphatidylcholine metabolite.
basic_science · Level V
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- Record sourced from PubMed, PMID 42556341.
- Also identified by DOI 10.1016/j.xcrm.2026.102970.
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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.