Preconceptional immunomodulation partially corrects pregnancy abnormalities induced by endometriosis in a mouse model, with normalization of transcriptional alterations observed in the developing fetal-maternal interface at the single cell level

K. Bouzid, Kheira Bouzid, R Bartkowski, Alix SILVERT, Fabiana Moresi, Camille Souchet, Marine Thomas, Isabelle Lagoutte, Vaarany Karunanithy, B Izac, Charles Chapron, Pietro Santulli, F. Batteux, Céline Méhats, Louis Marcellin, Ludivine Doridot
In: bioRxiv · 2026 · doi:10.64898/2026.01.02.695166 · W7118094282
article preprint OA: green CC0
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Preconceptional immunomodulation in a mouse model reduced endometriosis lesion size and corrected pregnancy complications, partially reversing endometriosis-induced transcriptional changes in the fetal-maternal interface.

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Abstract

Abstract Endometriosis is a chronic disease of gynaecological origin that affects approximately 10% of women worldwide and has a significant impact on patients’ lives. Women with endometriosis attempting to conceive may experience infertility and have a higher risk of obstetric complications. They are also more likely to miscarry and have placental defects during pregnancy. The impact of endometriosis on pregnancy remains unclear. Defects in implantation and placentation may be present, but these processes are difficult to study in human subjects. To address this issue, we used a surgically induced mouse model of endometriosis and examined pregnancy in the CBAxDBA crossbreed, which is commonly employed to study pregnancy immunology. We examined early (E9.5) and late (E18.5) gestational stages. In this model, we confirmed that the presence of endometriosis-like lesions resulted in fewer implantations and a higher proportion of fetal resorption, which is analogous to miscarriage. When an immune tolerance was induced previous to the endometriosis induction, we observed that endometriotic lesions were smaller, and gestational complications were mostly corrected. At early gestation (E9.5), fetal-maternal interfaces were retrieved to assess the potential impact of endometriosis and immunomodulation on placental development using single-cell RNA-sequencing. Our data show that most changes induced by endometriosis occur in decidual stromal cells, which originate from the endometrium. In these cells, we observed a consistent upregulation of Gata4, a transcription factor previously found to be elevated in the endometrium of women with endometriosis. We also observed downregulation of Prap1, which is an indicator of uterine receptivity and successful implantation in mice. In the mice where immune tolerance was induced, the endometriosis associated transcriptomic changes were partially reversed. In immune cells, endometriosis leads to an inflammation-associated signature. Additionally, the interferon gamma response is reduced in NK cells, which has been shown to be crucial for spiral artery remodelling and decidual integrity, which may be involved in the observed increased resorption rate. Overall, our findings provide new insights into endometriosis-associated infertility and pregnancy complications in a mouse model that can be partially corrected by immune modulation. These results suggest that targeting the immune system should be considered in future studies to improve pregnancy outcomes in patients with endometriosis.

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Condition tags

endometriosisinfertility

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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 (51)

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