Imbalance in the expression of the activating type I and the inhibitory type II interleukin 1 receptors in endometriosis
Imbalance in the expression of the activating type I and the inhibitory type II interleukin 1 receptors in endometriosis
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DOI：
10.1093/humrep/dem021
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发表时间：
2007-05-01
影响因子：
6.1
通讯作者：
Maheux, R.
中科院分区：
文献类型：
--
作者：
Akoum, Ali;Lawson, C.;Maheux, R.
背景：异位内膜组织的建立和发展依赖于它与新环境中存在的刺激的相互作用和反应。免疫细胞衍生的细胞因子，如白介素1(IL1)，可以单独或与雌激素共同作用，增强异位内膜细胞植入和发育到宿主组织的能力。本研究的目的是进一步探讨IL1受体I型(IL1R1)和IL1受体H型(IL1R2)在子宫内膜异位症/子宫内膜组织中的表达及意义。方法：采用免疫组织化学、免疫荧光染色、ELISA法、免疫印迹法、子宫内膜异位症细胞培养转染法。结果：我们的研究发现IL1R1和IL1R2在子宫内膜异位症患者的在位内膜组织中表达失衡，尤其是在异位内膜组织中。事实上，与正常妇女相比，IL1R2在子宫内膜异位症患者的在位和异位内膜中的表达明显降低，而在异位内膜组织中IL1R1的表达伴随着升高，尤其是在最初和最活跃的种植体中。结论：IL1R1/IL1R2失衡可能增强了子宫内膜细胞对IL1的反应性，可能是其植入和发育到宿主组织的关键机制之一。
BACKGROUND: 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 H (IL1R2), a potent and specific down-regulator of IL1 action, in normal compared to endometriotic/endometrial tissues. METHODS: Techniques included immunohistochemistry, immunofluorescent staining, ELISA, western blotting and endometriotic cell culture transfection. RESULTS: 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. CONCLUSIONS: 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.