Development and evaluation of two mouse models for endometriosis focused on the involvement of the immune system in endometriosis establishment

Natalia Nowak, Nowak, Nicola
2008 · doi:10.17169/refubium-12324 · W1777653212
other OA: green CC0 ⤵ 2 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-06 ⓘ

This study developed and evaluated two mouse models for endometriosis, finding that the injection model induced peritoneal inflammation and that a pre-inflamed environment reduced lesion burden, unlike immunosuppression.

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

This dissertation developed and evaluated two mouse models of endometriosis to study immune involvement in lesion establishment, using either an autologous transplantation approach (uterine biopsies sutured to peritoneum and intestine mesenteries) or an intraperitoneal injection approach with EGFP-expressing endometrial fragments. Histology showed lesions resembling human endometriotic lesions in both models, and the transplantation model displayed estrogen dependency via reduced lesion size after anti-estrogen treatment; a time-course in the injection model showed tissue reorganization and time-varying angiogenic processes. As a limitation, the models’ reproductive cycle differs from humans, and inflammatory effects were assessed in the peritoneal cavity rather than defining mechanistic immune pathways. Relevance to endometriosis: the entire work is centrally about endometriosis in mice, including experimentally probing peritoneal inflammation and immune suppression effects on lesion number and disease burden.

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Abstract

Endometriosis is a common gynaecological disease, affecting around 10 % of women in reproductive age. It is characterised by the presence of endometrial tissue fragments outside the uterine cavity, the so called endometriotic lesions, which grow in an estrogen-dependent manner. The major symptoms like severe chronic pain, dysmenorrhea and decreased fertility have a deep impact on the quality of the women’s lives. Current therapies result in pain release and amelioration of life conditions, but the recurrence rate is very high. Thus, there is an urgent need for new, more effective therapeutics. Due to ethical concerns, drug discovery cannot be conducted in humans. Non-human primates like the baboon, which menstruate and develop endometriosis spontaneously, are the best model system. However, high costs, long time periods until endometriosis occurs and ethical considerations limit the use of these animals. Mouse models are an alternative to examine endometriosis establishment and subsequently to test new therapeutical approaches, albeit their reproductive cycle is different. In the present work, two different endometriosis mouse models were established and evaluated to demonstrate their usability for endometriosis research and drug discovery. The first endometriosis model was an autologous transplantation model where uterus biopsies were sutured onto peritoneum and intestine mesenteries. Histological analysis revealed that the developed lesions resembled human endometriotic lesions. Additionally, the lesions demonstrated estrogen dependency by decreased lesion size after treatment with an anti-estrogen. Thus, the transplantation model is suitable for investigating anti-hormonal therapeutic approaches. The second endometriosis mouse model presented in this study was induced by intraperitoneal injection of enhanced green fluorescent protein- expressing endometrium fragments (EGFP). The developed lesions could be easily detected using a fluorescence microscope and revealed histological similarities with human lesions, thus making this model applicable for endometriosis research. Furthermore, a time course experiment demonstrated that the lesions underlay tissue reorganisation and angiogenic processes were visible which varied over time. In the pathophysiology of endometriosis, one important aspect is the role of the immune system, even though its exact impact still remains enigmatic. In the present study, both models were investigated particularly with regard to inflammatory events in the peritoneal cavity. No differences could be demonstrated for the transplantation model compared to sham-operated and untreated controls. However, in the injection model increased inflammatory parameters could be detected 24 h, 72 h and even 10 days after endometriosis induction. Thus, the induction of endometriosis provoked a peritoneal inflammation in the injection model. Furthermore, the injection model was used to examine the impact of an altered immune system on endometriosis establishment. Endometriosis was induced on the one hand in a pre-inflamed peritoneal cavity and on the other hand in immunosuppressed animals. Induction of endometriosis in a pre-inflamed peritoneal cavity resulted in fewer lesions and significantly lower disease burden per mouse. Thus, a pre-existing peritoneal inflammation might not be a factor favouring the development of endometriosis. By contrast, a suppressed immune system had no significant impact on lesion number and size. In summary, the injection model can be used to investigate establishment of lesions and potentially attachment-interfering agents.

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endometriosisdysmenorrhea

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