Toros University, Vocational School, Medical Services and Techniques, Mersin, Turkey.
Çukurova University, Faculty of Medicine, Pathology Department, Adana, Turkey.
J Gynecol Obstet Hum Reprod. 2021 May;50(5):101971. doi: 10.1016/j.jogoh.2020.101971. Epub 2020 Nov 2.
Endometriosis is a gynocological disease characterized by the presence of the endometrial glands and stroma outside the uterine cavity. This disease affects % 6-10 of women with reproductive age and it causes serious problems such as pelvic pain, dysmenorrhea and infertility. Although endometriosis is one of the most investigated disease of gynecology, its pathogenesis is not clear completely. In recent years, many studies revealed the inflammatory nature of endometriosis. Many of the immune cells and their secretory products cytokines and chemokines has been detected in body fluids of women with endometriosis. Cytokines are protein or glycoprotein in structures and hormon-like molecules that act generally in a paracrine fashion to regulate immun responses. They involved in chemotaxis, cell proliferation, cell activation, motility, adhesion and morphogenesis. Tumor necrosis factor alpha (TNF-α) is a proinflammatory cytokine secreted by the macrophages, monocytes, neutrophiles, T cells and natural killer cells. It stimulates increase in the level of the chemokines in body fluids. Monocyte chemotactic protein 2 (MCP-2) is a chemokine act to recruit and activate monocytes into sites of inflammation area. The aim of this study to investigate the ultrastructural properties and whether the expression and localization of TNF-α and MCP-2 in the eutopic endometrium (normal endometrium of women with endometriosis) and endometritic tissues of women with endometriosis. Eutopic endometrial and endometriotic tissue samples were obtained from women with endometriosis between 20-41 y and normal endometrial tissues were collected from 5 women without endometriosis as a control group. Tissues were processed for light and electron microscopy and examined. The epithelial cells of endometriotic tissues were revealed strongly cytoplasmic TNF-α and MCP-2 immunreactivities. Eutopic endometrial tissues were also stained prominently for both TNF-α and MCP-2. Furthermore, a significant increase in stromal macrophages were observed in endometriotic tissues. Moreover, the ultrastructural observations on the normal and endometriotic tissues were exhibited microvilli-rich cells and ciliated cells. These findings suggest that TNF-α and MCP-2 may be involved in normal endometrial biology and in the pathogenesis of endometriosis.
子宫内膜异位症是一种妇科疾病,其特征是子宫内膜腺体和基质出现在子宫腔外。这种疾病影响生育年龄的女性的 6-10%,并导致严重问题,如盆腔疼痛、痛经和不孕。尽管子宫内膜异位症是妇科最受研究的疾病之一,但它的发病机制尚不完全清楚。近年来,许多研究揭示了子宫内膜异位症的炎症性质。在患有子宫内膜异位症的女性的体液中已经检测到许多免疫细胞及其分泌产物细胞因子和趋化因子。细胞因子是结构上的蛋白质或糖蛋白,是类似激素的分子,通常以旁分泌的方式发挥作用,调节免疫反应。它们参与趋化、细胞增殖、细胞激活、运动、黏附和形态发生。肿瘤坏死因子-α(TNF-α)是巨噬细胞、单核细胞、中性粒细胞、T 细胞和自然杀伤细胞分泌的促炎细胞因子。它刺激体液中趋化因子水平的增加。单核细胞趋化蛋白 2(MCP-2)是一种趋化因子,可招募并激活单核细胞进入炎症区域。本研究旨在探讨 TNF-α 和 MCP-2 在子宫内膜异位症患者的在位子宫内膜(子宫内膜异位症患者的正常子宫内膜)和子宫内膜组织中的超微结构特性以及表达和定位。从患有子宫内膜异位症的 20-41 岁女性中获取在位子宫内膜和子宫内膜组织样本,并从 5 名无子宫内膜异位症的女性中收集正常子宫内膜组织作为对照组。对组织进行光镜和电镜检查。结果显示,子宫内膜异位症组织的上皮细胞显示出强烈的细胞质 TNF-α 和 MCP-2 免疫反应性。在位子宫内膜组织也明显染色 TNF-α 和 MCP-2。此外,在子宫内膜异位症组织中观察到基质巨噬细胞显著增加。此外,对正常和子宫内膜异位症组织的超微结构观察显示出富含微绒毛的细胞和纤毛细胞。这些发现表明,TNF-α 和 MCP-2 可能参与正常子宫内膜生物学和子宫内膜异位症的发病机制。