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Volume 30, Issue 167, January 2026

The role of the gut and reproductive tract microbiota in the development, diagnosis, and treatment of endometriosis

Malinowski M1♦, Krasowski M2, Kalinowska A1, Pietras W1, Koziel A1, Kurek Z1, Jentkiewicz A1, Haj Obeid E1, Ulrych J1, Krupa J1

1Medical University of Warsaw, 61 Żwirki i Wigury Street, 02-091 Warsaw, Poland
2Poznań University of Medical Science, 10 Fredry Street, 61-701 Poznan, Poland

♦Corresponding author
Maciej Malinowski, Medical University of Warsaw, 61 Żwirki i Wigury Street, 02-091 Warsaw, Poland

ABSTRACT

Endometriosis is an inflammatory disorder. Caused by the proliferation of endometrial tissue outside the uterine mucosa. Progression results from elaborate interactions among hormonal, immunological, and environmental factors. Growing evidence indicates that the gut and reproductive tract microbiota play a key role in the pathogenesis of endometriosis. In patients with endometriosis, an increase in potentially pathogenic taxa, including Escherichia, Gardnerella, and Streptococcus, is observed. Dysbiosis leads to the translocation of bacterial endotoxins (Lipopolysaccharide (LPS)), activation of the TLR4/NF-κB pathway, and increased production of pro-inflammatory cytokines (IL-6, IL-8, TNF-α), which promote angiogenesis and the proliferation of endometrial foci. Furthermore, disturbances in the activity of the enzyme β-glucuronidase, part of the oestrobolome, increase the pool of active oestrogens, playing a role in disease progression. Despite the growing number of studies, further prospective studies involving larger populations are needed to standardise diagnostic methods and confirm the therapeutic potential of microbiome modulation in treating endometriosis.

Keywords: endometriosis, gut microbiota, reproductive tract microbiota, estrabolome

Medical Science, 2026, 30, e9ms3757
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DOI: https://doi.org/10.54905/disssi.v30i167.e9ms3757

Published: 21 January 2026

Creative Commons License

© The Author(s) 2026. Open Access. This article is licensed under a Creative Commons Attribution License 4.0 (CC BY 4.0).