Laboratory of Immunology, EA 1833, Université Paris Descartes, Hôpital Cochin, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France; Department of Digestive and Endocrine Surgery, Université Paris Descartes, Hôpital Cochin, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France.
Laboratory of Immunology, EA 1833, Université Paris Descartes, Hôpital Cochin, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France.
J Reprod Immunol. 2014 Jun;103:45-52. doi: 10.1016/j.jri.2013.12.121. Epub 2014 Jan 23.
Immunological and angiogenetic factors enhance the implantation of endometrial cells in the peritoneal cavity. The aim of this work was to determine the role of the CXCL12-CXCR4 axis in the attraction and the peritoneal implantation of endometriotic stromal cells in deep infiltrating endometriosis (DIE). Biopsies of DIE nodules were obtained from 14 patients undergoing surgical treatment for DIE with low rectal involvement and from 12 patients without macroscopic endometriosis undergoing laparoscopy. CXCR4 expression was evaluated by Western blot analysis and flow cytometry in eutopic endometrial cells and DIE stromal cells in primary cultures derived from the biopsies. CXCL12-induced migration of DIE eutopic endometrial stromal cells was evaluated by transwell migration. CXCL12 was assayed in peritoneal fluids by ELISA. CXCR4 expression was higher in eutopic endometrial stromal cells than in control endometrial cells (p<0.05) and in DIE stromal cells (p<0.05). Eutopic endometrial stromal cells were more attracted by CXCL12 than control cells (p<0.01). CXCL12 was higher in DIE peritoneal fluids than in controls (p<0.05). CXCR4 was down-regulated in deep infiltrating endometriotic stromal cells. The CXCL12-CXCR4 axis plays a role in the attraction of eutopic endometrial cells into the peritoneal cavity, and the down-regulation of CXCR4 in resident endometriotic cells could cause their arrest in situ.
免疫和血管生成因素增强了子宫内膜细胞在腹腔内的植入。本研究旨在确定 CXCL12-CXCR4 轴在吸引和腹膜内种植子宫内膜异位症间质细胞（DIE）中的作用。从 14 例接受手术治疗的 DIE 患者（低位直肠受累）和 12 例无肉眼子宫内膜异位症的患者（接受腹腔镜检查）的 DIE 结节活检中获得了标本。通过 Western blot 分析和流式细胞术评估了原发性培养物中在位子宫内膜细胞和 DIE 间质细胞中 CXCR4 的表达。通过 Transwell 迁移评估了 CXCL12 诱导的 DIE 在位子宫内膜间质细胞的迁移。通过 ELISA 检测腹腔液中的 CXCL12。与对照组子宫内膜细胞（p<0.05）和 DIE 间质细胞（p<0.05）相比，在位子宫内膜间质细胞中 CXCR4 的表达更高。与对照组细胞相比，CXCL12 更能吸引在位子宫内膜间质细胞（p<0.01）。DIE 腹腔液中的 CXCL12 高于对照组（p<0.05）。深浸润性子宫内膜异位症间质细胞中 CXCR4 下调。CXCL12-CXCR4 轴在吸引在位子宫内膜细胞进入腹腔中起作用，驻留的子宫内膜异位症细胞中 CXCR4 的下调可能导致它们在原位停滞。
