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In the United Kingdom, approximately 1.5 million women and individuals assigned female at birth are currently affected by endometriosis [1]. This condition manifests with a range of symptoms, including chronic pelvic pain, fatigue, depression, and infertility, which can contribute to significant social and relationship challenges [1,2]. Despite the high prevalence of endometriosis, delays in diagnosis and treatment [2] highlight the urgent need for research into its underlying aetiology. Endometriosis is classified into three primary types: peritoneal, ovarian, and deep infiltrative, each characterized by the presence of ectopic endometrial tissue in specific anatomical locations.
The exact cause if endometriosis is unknown, but is thought to be multifactorial, including: retrograde menstruation, genetics, lymphatic or circulatory spread, immunodeficiency, metaplasia and the environment [2]. Muraoka et al (2023) conducted a comparative analysis of fibroblasts within the endometrial stroma of patients with and without endometriosis, investigating their potential association with Fusobacterium spp. They firstly identified 10 genes that were upregulated and 3 genes within fibroblasts that were downregulated in endometriosis samples compared to control samples [3]. Notably, the expression of transgelin (TAGLN) proteins, which promote fibroblast proliferation and mobility as well as endometrial cell proliferation via IL-6, was significantly increased in fibroblasts from endometriosis patients [3,4]. TGF-β1, a key growth factor implicated in endometriosis, is known to induce myofibroblast-associated genes, including TAGLN [3,4].
The research team then used fluorescence in situ hybridization (FISH) to detect the presence of bacteria in endometrial samples from both patient sets, finding Fusobacterium spp [3]. in 64.3% of endometrial tissue samples and 52.4% of endometriotic tissue samples of patients with endometriosis, compared to 7.1% in controls [3]. This suggests that Fusobacterium spp. infiltration may lead to the recruitment of macrophages within endometriotic lesions. They observed increased macrophage infiltration, including CD163-positive M2 macrophages known to produce TGF-β1, in the endometrial tissues of endometriosis patients [3].
To further elucidate this relationship, the researchers used a mouse model, inoculating the mice with F. nucleatum. This resulted in a significant increase in TAGLN-positive myofibroblasts and a corresponding increase in the number and weight of endometriotic lesions. The findings of this study suggest a potential therapeutic approach for endometriosis by targeting F. nucleatum infiltration in the endometrium with antibiotic therapies.
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Written by DWS Microbiologist, Charlotte Austin
References
- Endometriosis UK (2024) What is Endometriosis? https://www.endometriosis-uk.org/what-endometriosis
- Senat, H., Grabowska, P., Senat, A., Bolla, P., Madej, A., Marczyńska, Z., & Libracka, K. (2024). Endometriosis: Pathogenesis, diagnosis, treatment and the role of gut microbiota. Journal of Education, Health and Sport, 59, 87–101.
- Muraoka, A., Suzuki, M., Hamaguchi, T., Watanabe, S., Iijima, K., Murofushi, Y., Shinjo, K., Osuka, S., Hariyama, Y., Ito, M., Ohno, K., Kiyono, T., Kyo, S., Iwase, A., Kikkawa, F., Kajiyama, H., & Kondo, Y. (2023). Fusobacterium infection facilitates the development of endometriosis through the phenotypic transition of endometrial fibroblasts. Science translational medicine, 15(700)
- Ghosh, A.; Jaaback, K.; Boulton, A.; Wong-Brown, M.; Raymond, S.; Dutta, P.; Bowden, N.A.; Ghosh, A. (2024) Fusobacterium nucleatum: An Overview of Evidence, Demi-Decadal Trends, and Its Role in Adverse Pregnancy Outcomes and Various Gynecological Diseases, including Cancers. Cells, 13, 717
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