Gut microbiota and microbiota-derived metabolites promotes endometriosis

Sangappa B Chadchan, Sumanta Kumar Naik, Pooja Popli, Chandni Talwar, Satwikreddy Putluri, Chandrasekhar R Ambati, Michael A Lint, Andrew L Kau, Christina L Stallings, Ramakrishna Kommagani
Cell death discovery · 2023 · vol. 9(1) , pp. 28 · doi:10.1038/s41420-023-01309-0 · PMID:36693853 · PMC9873805 · W4317889673
article OA: gold CC0 ⤵ 38 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Gut microbiota transplantation in mice with endometriosis restored lesion growth, which was promoted by the metabolite quinic acid, suggesting the gut microbiome and its metabolites contribute to disease progression.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-09 ⓘ

The paper investigated whether gut microbiota causally affects endometriosis progression by using antibiotic-induced microbiota-depleted (MD) mice and comparing endometriotic lesion growth to control mice, with microbiota depletion confirmed by fecal qPCR and associated immune/intestinal phenotypes. MD mice showed reduced endometriotic lesion growth, and oral transplantation of feces from mice with endometriosis rescued lesion growth, while experiments with germ-free donor mice indicated uterine microbiota is dispensable for lesion growth. The authors also reported that gut microbiota altered peritoneal immune cell populations and identified a fecal metabolite signature linked to endometriosis; one metabolite, quinic acid, promoted endometriotic epithelial cell survival in vitro and lesion growth in vivo. The paper explicitly notes the major limitation that its translational implications for diagnosis rely on whether these metabolite signatures are recapitulated in humans. This paper is centrally about endometriosis — it tests causal roles for gut microbiota and microbiota-derived metabolites (including quinic acid) in endometriotic lesion growth in mice and links these metabolites to potential stool-based diagnostics.

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Abstract

Endometriosis is a pathological condition of the female reproductive tract characterized by the existence of endometrium-like tissue at ectopic sites, affecting 10% of women between the age 15 and 49 in the USA. However, currently there is no reliable non-invasive method to detect the presence of endometriosis without surgery and many women find hormonal therapy and surgery as ineffective in avoiding the recurrences. There is a lack of knowledge on the etiology and the factors that contribute to the development of endometriosis. A growing body of recent evidence suggests an association between gut microbiota and endometriosis pathophysiology. However, the direct impact of microbiota and microbiota-derived metabolites on the endometriosis disease progression is largely unknown. To understand the causal role of gut microbiota and endometriosis, we have implemented a novel model using antibiotic-induced microbiota-depleted (MD) mice to investigate the endometriosis disease progression. Interestingly, we found that MD mice showed reduced endometriotic lesion growth and, the transplantation of gut microbiota by oral gavage of feces from mice with endometriosis rescued the endometriotic lesion growth. Additionally, using germ-free donor mice, we indicated that the uterine microbiota is dispensable for endometriotic lesion growth in mice. Furthermore, we showed that gut microbiota modulates immune cell populations in the peritoneum of lesions-bearing mice. Finally, we found a novel signature of microbiota-derived metabolites that were significantly altered in feces of mice with endometriosis. Finally, we found one the altered metabolite, quinic acid promoted the survival of endometriotic epithelial cells in vitro and lesion growth in vivo, suggesting the disease-promoting potential of microbiota-derived metabolites. In summary, these data suggest that gut microbiota and microbiota-derived metabolome contribute to lesion growth in mice, possibly through immune cell adaptations. Of translational significance, these findings will aid in designing non-invasive diagnostics using stool metabolites for endometriosis.

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endometriosis

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