Abstract
Endometriosis is a chronic inflammatory condition characterised by the growth of endometrial epithelial and stromal cells outside the uterine cavity. In addition to Sampson’s theory of retrograde menstruation, endometriosis pathogenesis is facilitated by a privileged inflammatory microenvironment, with T regulatory FoxP3+ expressing T cells (Tregs) being a significant factor. PreImplantation Factor (PIF) is a peptide essential for pregnancy recognition and development. An immune modulatory function of the synthetic PIF analog (sPIF) has been successfully confirmed in multiple animal models. We report that PIF is expressed in the epithelial ectopic cells in close proximity to FoxP3+ stromal cells. We provide evidence that PIF interacts with FoxP3+ cells and modulates cell viability, dependent on cell source and presence of inflammatory mediators. Our finding represent a novel PIF-based mechanism in endometriosis that has potential for novel therapeutics.
Highlights
Endometriosis is a chronic, benign disease affecting 10% of women in their reproductive years and characterized by the presence of stromal and epithelial cells outside the uterine cavity [1]
To determine the role of PreImplantation Factor (PIF) in endometriosis, tissue samples were obtained from women with or without endometriosis including the ectopic ovarian endometriomas and peritoneal implants during the proliferative and secretory phases
To elucidate the potential role of PIF in endometriosis we used epithelial cell lines isolated from the eutopic endometrium (EM E6/E7) [39] and ectopic endometriomas (EM’osis) [40] and primary endometrial stromal cells (ESC) from women with and without endometriosis
Summary
Endometriosis is a chronic, benign disease affecting 10% of women in their reproductive years and characterized by the presence of stromal and epithelial cells outside the uterine cavity [1]. Endometriosis lesions are found predominantly in the pelvis, potentially through the reflux of viable endometrial cells during retrograde menstruation [1, 2]. Recent evidence suggests that the pathogenesis of endometriosis requires more than retrograde menstruation, underlying the emerging role of stems cells and the immune response [3,4,5]. The cyclic regeneration of a healthy endometrium depends on stem cells. Both endometrial- and bone marrow-derived stem cells may migrate to ectopic lesions and contribute to lesion growth [3]. Irrespective of their source once endometrial cells are present they
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