Endometriosis: A key to its progression in the gut microbiota?
While endometriosis affects 10% of women of childbearing age, it remains poorly understood and difficult to treat. A study on mice advances our understanding of the disease, highlighting the involvement of the gut microbiota and its metabolites in the progression of endometriosis.
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Despite decades of research on endometriosis, the means of providing relief are limited for patients who experience recurring issues despite hormone therapy or surgical removal of lesions. The factors contributing to the development of the disease remain poorly understood. Retrograde menstruation towards the peritoneal cavity, which affects 90% of women, is not eliminated by immune cells in 10% of them. The endometrial tissue is then believed to proliferate under the influence of inflammatory cytokines and growth factors, leading to the formation of ectopic lesions. In addition, a growing number of studies on patients highlights the role of the gut microbiota: could the gut dysbiosis observed and the role of gut metabolites be involved in the pathophysiology and progression of endometriosis?
The gut microbiota: A factor in the progression of endometriosis lesions
To explore the role of the gut microbiota in the progression of endometriosis, researchers have developed a new mouse model of endometriosis in which (sidenote: These mice have less bacteria in their gut microbiota compared to the control mice. ) .The first finding: the depletion of the gut microbiota does not have a harmful effect on the general uterine morphology. However, the growth of endometriosis lesions is reduced in the DM mice compared to endometriosis mouse models whose gut microbiota has not been depleted. Fecal microbiota transplantation (FMT) from these control mice to the DM mice resulted in a resumption of endometriosis lesion growth, whereas another experiment with FMT from healthy mice (without endometriosis, with non-depleted gut microbiota) did not result in this resumption of growth. This confirms that the gut microbiota is essential for the growth of endometriosis lesions.
10% Endometriosis affects 10% of women of childbearing age.
A bacterial metabolite promotes the survival of endometrial cells
Another finding is that the uterine microbiota is not necessary for lesion growth. Researchers also suppose that the gut microbiota has an impact on the growth of endometriosis lesions through modulation of the peritoneal immune cells. Finally, they identify an intestinal metabolic signature specific to endometriosis. One of the metabolites, quinic acid, promotes the survival of endometrial epithelial cells in vitro, and the growth of lesions in vivo.
These results suggest that the gut microbiota and its metabolome contribute to the growth of endometriosis lesions in mice, possibly through the modulation of certain immune cell populations. These results could be useful for the development of tools for the early diagnosis of the disease and for assessing its progression.
