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

The paper investigates how gut microbiota influences endometriosis pathogenesis using two mouse models: human fecal microbiota transplantation from endometriosis patients versus controls, and an autograft-derived endometriosis model combined with antibiotic-induced microbiota perturbation. In the FMT model, mice receiving microbiota from endometriosis patients showed more pain behaviors and worse lesion burden, alongside reduced M1-associated CD86 MFI with no clear change in CD206; in the antibiotic/metronidazole model, metronidazole treatment lessened pain and disease severity and was associated with reduced lesion size/weight and a shift in macrophage phenotypes (decreased CD206+ M2 with only marginal increases in CD86+ M1). Strain-resolved metagenomics and correlations implicated Parabacteroides goldsteinii as inversely associated with multiple EMS severity indices, supported by increased Pg with metronidazole and decreased Pg in feces from EMS patients, though the excerpted text leaves downstream mechanistic causality to later sections. This paper is centrally about endometriosis — it tests Parabacteroides goldsteinii (and its metabolite 7-KLCA) as a microbiota-driven regulator that attenuates endometriosis via TGR5 and macrophage reprogramming through the PPARγ/GPR132 axis.

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