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Observational analysis identifies distinct immune cell populations in menstrual effluent, suggesting altered cellular pathways in endometriosis.
Endometriosis is a chronic gynecological disease affecting 1 in 10 reproductive-aged women and is characterized by the ectopic presence of endometrial tissue outside the uterus. The leading hypothesis for disease etiology is via the reflux of menstrual effluent (ME) into the peritoneal cavity. ME is a complex mixture of viable endometrial tissue, proteins, and immune cells which serve specialized functions during menstruation to support and repair the endometrium. We hypothesized shifts in the subpopulations of immune cells present during retrograde menstruation may alter the microenvironment of the peritoneal cavity leading to a favorable environment for uterine tissue attachment and survival of endometriotic lesions. Menstrual effluent collected on days 1 and 2 of menstruation identified from women with endometriosis distinct morphological features, increased subpopulations of aged neutrophils, increased anti-inflammatory macrophages, and overall impaired clearance pathways that hijack endometrial clearance likely contributing to the development and progression of endometriosis.
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Wilson et al. (2025) studied this question.
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