Akoum Ali, Lawson C, Herrmann-Lavoie C, Maheux R
Unité d'Endocrinologie de la Reproduction, Centre de Recherche, Hôpital Saint-François d'Assise, Centre Hospitalier Universitaire de Québec, Canada.
Hum Reprod. 2007 May;22(5):1464-73. doi: 10.1093/humrep/dem021. Epub 2007 Feb 26.
The ectopic establishment and progression of endometrial tissue is dependent upon its interaction with and responsiveness to the stimuli present in its new environment. Immune cell-derived cytokines, such as interleukin 1 (IL1), may alone or in concert with estrogens enhance the capability of ectopic endometrial cells to implant and develop into the host tissue. The objective of this study was to further evaluate the expression and significance of IL1 receptor type I (IL1R1), the signalling receptor that mediates cell activation by IL1, and IL1 receptor type II (IL1R2), a potent and specific down-regulator of IL1 action, in normal compared to endometriotic/endometrial tissues.
Techniques included immunohistochemistry, immunofluorescent staining, ELISA, western blotting and endometriotic cell culture transfection.
Our study showed an imbalance in the expression of IL1R1 and IL1R2 in eutopic, and particularly in ectopic, endometrial tissues of women with endometriosis. Actually, a decreased IL1R2 expression is predominant in the eutopic and ectopic endometrium of women with endometriosis when compared with normal women, whereas a concomitant increase in IL1R1 expression occurs in ectopic endometrial tissue in comparison to eutopic endometrial tissue of normal or endometriotic women, particularly in the initial and most active implants. Transfection of endometriotic cells with a cDNA coding for IL1R2 resulted in a significant decrease in IL1-induced secretion of vascular endothelial cell growth factor and monocyte chemotactic protein 1.
IL1R1/IL1R2 imbalance may amplify endometrial cell responsiveness to IL1 and represent a key mechanism underlying the ability of these cells to implant and develop into host tissues.
子宫内膜组织的异位植入和进展取决于其与新环境中存在的刺激因素的相互作用及其对这些刺激的反应能力。免疫细胞衍生的细胞因子，如白细胞介素1（IL1），可能单独或与雌激素协同作用，增强异位子宫内膜细胞植入并发育成宿主组织的能力。本研究的目的是进一步评估I型白细胞介素1受体（IL1R1，介导IL1激活细胞的信号受体）和II型白细胞介素1受体（IL1R2，IL1作用的有效且特异性下调因子）在正常子宫内膜组织与子宫内膜异位症/子宫内膜组织中的表达及意义。
技术包括免疫组织化学、免疫荧光染色、酶联免疫吸附测定、蛋白质印迹法和子宫内膜异位细胞培养转染。
我们的研究表明，在患有子宫内膜异位症的女性的在位内膜，尤其是异位内膜组织中，IL1R1和IL1R2的表达失衡。实际上,与正常女性相比，IL1R2表达降低在患有子宫内膜异位症的女性的在位内膜和异位内膜中占主导，而与正常或患有子宫内膜异位症的女性的在位内膜组织相比，IL1R1表达在异位内膜组织中增加，尤其是在最初且最活跃的植入部位。用编码IL1R2的cDNA转染子宫内膜异位细胞导致IL1诱导的血管内皮细胞生长因子和单核细胞趋化蛋白1的分泌显著减少。
IL1R1/IL1R2失衡可能会放大子宫内膜细胞对IL1的反应性，并代表这些细胞植入并发育成宿主组织能力的关键机制。
