The histopathological features of the surgical endometriosis model using systemic autoimmune disease-prone mice

Marina Hosotani, Machiko Akita, Hiromi Ueda, Takafumi Watanabe
The Journal of veterinary medical science · 2022 · vol. 85(1) , pp. 1–8 · doi:10.1292/jvms.22-0442 · PMID:36436950 · PMC9887222 · W4310335125
article OA: gold CC0 ⤵ 3 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This study established a surgical endometriosis model in autoimmune-prone mice, finding distal lesions only in MRL/lpr mice and altered T cell infiltration in transplanted endometrium, suggesting endogenous T cells affect ectopic endometrial growth.

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

The study aimed to characterize histopathological features of a surgical endometriosis rodent model to probe how systemic autoimmune disease susceptibility relates to endometriosis development. Uterine tissues from MRL/MpJ-Faslpr/lpr (MRL/lpr) or MRL/+ donor mice were transplanted into peritoneal recipients, producing proximal lesions near the transplantation point and distal lesions in more distant sites. Distal lesions occurred only in MRL/lpr mice, while lesion histology and the distribution of sex hormone receptors and T cells in the endometriosis lesions themselves showed no genotype- or region-related differences; however, transplanted uterine tissues in MRL/lpr donors showed large T-cell infiltration in the lamina propria and recipients exhibited splenomegaly more often. This paper is centrally about endometriosis — it establishes and examines histopathology of a surgical endometriosis model in autoimmune-prone mice and links endogenous T-cell infiltration to lesion growth patterns.

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Abstract

Endometriosis is a common gynecological disease that affects women of reproductive age in which the uterine endometrium grows outside the uterus. Origin of the ectopic endometrium is thought to be the retrograde endometrium through the oviducts. However, factors that determine the adherence and proliferation of the ectopic endometrium have not been revealed. Importantly, systemic autoimmune diseases are considered a key factor in the endometriosis onset. Herein, we established a surgical endometriosis rodent model using autoimmune disease-prone MRL/MpJ-Faslpr/lpr (MRL/lpr) and MRL/+ mice to provide basic evidence of the relationship between autoimmune disease and endometriosis. Endometriosis lesions were successfully induced in two regions after transplanting uterine tissues from donor mice into the peritoneal cavity of recipient mice: the peritoneum or adipose tissue around the transplantation point (proximal lesions) and the gastrosplenic ligament or intestinal mesentery far from the transplantation site (distal lesions). Distal lesions were observed only in MRL/lpr mice, whereas endometriosis lesions showed no genotype- or region-related differences in the histology and distribution of sex hormone receptors and T cells. In contrast, transplanted uterine tissues in donor MRL/lpr mice exhibited a large infiltration of T cells in the lamina propria. Splenomegaly was more common in recipient than that in donor MRL/lpr mice. These results suggest that the infiltration of endogenous T cells in the endometrium alters the growth features of ectopic endometrium, possibly affecting the severity of endometriosis in patients with systemic autoimmune diseases.

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Condition tags

endometriosis

MeSH descriptors

Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases Autoimmune Diseases

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