Current understanding of the connection between endometriosis and intestinal microbiocenosis: a literature review

Marina Sergeevna Shelekhova, Anna Nikolayevna Modorskaya, Angelina Nikolayevna Fil'chakova, Yuliya Viktorovna Grudkova, Kirill Pavlovich Rayevskiy
In: Russian Medicine · 2024 · vol. 30(2) , pp. 181–190 · doi:10.17816/medjrf626841 · W4396515251
review OA: hybrid CC0
🔓 Open OA copy View on OpenAlex View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This literature review found that endometriosis is linked to intestinal dysbiosis, characterized by reduced Lactobacillus and increased harmful bacteria, which promotes inflammation and estrogen metabolism.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-08 ⓘ

This 2024 literature review examines studies on how intestinal microbiocenosis and dysbiosis may contribute to endometriosis pathogenesis, summarizing reported shifts in gut microbial taxa, immune and inflammatory signaling, estrogen metabolism, and related molecular pathways. Across cited research, the review highlights patterns such as reduced Lactobacillus alongside increased potentially harmful groups, alterations in the Firmicutes-to-Bacteroidetes ratio, links to higher TNF-α, NF-κB, and IL-8, and associations with apoptosis/proliferation/angiogenesis factors (e.g., Fas/Bax, EGFR, VEGF), while also describing microbiota-derived enzymes (β-glucuronidase, β-glucosidase) that may increase free estrogen. As a limitation, the paper emphasizes that additional research is still needed to fully clarify the mechanisms and includes heterogeneous findings (e.g., some studies reporting no effect on intestinal diversity). This paper is centrally about endometriosis — it reviews evidence connecting intestinal microbiocenosis and dysbiosis to endometriosis development and progression.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Endometriosis is a complex condition that affects at least 10% of women in their reproductive years worldwide. It is characterized by persistent pelvic pain, dysmenorrhea, impaired pelvic organ function, infertility, and psychological distress. Alarmingly, about 30% of patients experience a recurrence of the disease even after receiving full treatment. Given the urgent nature of this problem, extensive studies are regularly conducted to investigate the various factors that contribute to the development of endometriosis. One area of particular interest is the relationship between the condition and changes in the intestinal microflora. Research suggests that endometriosis is primarily associated with a decrease in the number of Lactobacillus bacteria and an increase in the presence of potentially harmful flora, including Enterobacteriaceae, Bifidobacterium, Parabacteroides, Proteobacteria, Actinobacteria, Cyanobacteria, Saccharibacteria, Fusobacteria etc. Furthermore, there is a focus on the ratio of Firmicutes to Bacteroidetes. Such dysbiosis leads to abnormal cytokine expression and immune cell dysfunction, ultimately resulting in chronic inflammation. A correlation has been found between changes in the intestinal microflora in endometriosis and an increase in the levels of TNF-α, NF-κB, and IL-8. Additionally, the condition has been linked to factors related to apoptosis (Fas and Bax), proliferation (epidermal growth factor), and angiogenesis (VEGF). Another significant aspect is the role of the intestinal microbiota in the breakdown of estrogen. Enzymes such as β-glucuronidase and β-glucosidase, secreted by the microbiota, contribute to the breakdown of estrogen and subsequently increase the levels of free estrogen in the bloodstream. This increase in free estrogen is believed to play a role in the development of endometriosis by promoting the proliferative activity of endometrial cells. It further confirms the significance of intestinal dysbiosis in the pathogenesis of the disease. However, despite these findings, additional research is still required to fully understand the mechanisms behind the development of endometriosis.

My notes (saved in your browser only)

Condition tags

endometriosisdysmenorrheainfertility

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (50)

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0 · commercial use OK