国际妇产科学杂志

国际妇产科学杂志 ›› 2020, Vol. 47 ›› Issue (5): 485-489.

• 普通妇科疾病及相关研究 综述 •    下一篇

Toll样受体4介导子宫内膜异位症发病机制的研究进展

郭灵，程忠平   

  1. 200072上海，南京医科大学上海十院临床医学院
  • 收稿日期:2020-03-28 修回日期:2020-05-23 出版日期:2020-10-15 发布日期:2020-10-27
  • 通讯作者: 程忠平，E-mail：mdcheng@tongji.edu.cn E-mail:mdcheng@tongji.edu.cn

Advances in Mechanism of TLR4 Mediating Endometriosis

GUO Ling, CHENG Zhong-ping   

  1. Clinical Medical College of Shanghai Tenth People′s Hospital of Nanjing Medical University, Shanghai 200072, China
  • Received:2020-03-28 Revised:2020-05-23 Published:2020-10-15 Online:2020-10-27
  • Contact: CHENG Zhong-ping, E-mail: mdcheng@tongji.edu.cn E-mail:mdcheng@tongji.edu.cn

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摘要： 子宫内膜异位症（Endometriosis，EMs）常见于育龄期女性，可导致患者痛经、下腹痛，甚至不孕。研究表明EMs的发病除受激素影响外，也与慢性炎症相关。Toll样受体4（Toll-like receptor 4，TLR4）是一种在机体固有免疫应答及抗病原体免疫中发挥重要作用的炎症介质，存在于子宫内膜细胞，可能在EMs的发生、发展中扮演关键角色。女性月经期来自下生殖道的病原体及脱落的子宫内膜组织碎片随逆行经血进入上生殖道，病原体激活异位子宫内膜细胞上的TLR4信号通路，招募和激活免疫细胞（如巨噬细胞等），引发局部炎症反应，促进不同的炎症因子和生长因子分泌，并刺激子宫内膜细胞增殖；持续的炎症损伤使受损细胞产生应激反应释放其他内源性配体[如热休克蛋白70（HSP70）、高迁移率族蛋白B1（HMGB-1）等]，又进一步激活TLR4信号通路。以上两种反应互相累加使炎症微环境不断激活，从而促进子宫内膜细胞的黏附、侵袭和增殖，最终导致EMs的发生和发展。该理论提示针对TLR4信号通路的抗炎治疗或可成为治疗EMs的新方向。

关键词: 子宫内膜异位症；, 炎症；, 应激反应；, Toll样受体4；, TLR4信号通路

Abstract: Endometriosis(EMs) is a common disease in fertile women，leading to dysmenorrhea, pelvic pain and even infertility. Recent studies have indicated that the pathogenesis of EMs is not only affected by hormones, but also associated with chronic inflammation. Toll like receptor 4 (TLR4), a kind of inflammatory mediators existing in endometrial cells, plays an important role in host innate immunity against pathogen. It may be pivotal in the occurrence and development of EMs. During menstruation, pathogens from the lower genital tract and the shed endometrial tissue fragments enter the upper genital tract with retrograde menstruation. Pathogens activate TLR signal pathway on ectopic endometrial cells, recruit and activate immune cells (e.g. macrophages etc.) to trigger local inflammatory response and promote the secretion of different inflammatory factors and growth factors, thus stimulate the proliferation of endometrial cells. The sustained inflammatory damage causes the injured cells to induce stress reaction and release other endogenous ligands (e.g. HSP70, HMGB-1, etc.), so that TLR4 signal pathway could be further activated. The joint effect of above two reactions activate the inflammatory microenvironment to promote the adhesion, invasion and proliferation of endometrial cells, and ultimately lead to the occurrence and development of EMs. This theory suggests that anti-inflammatory remedy against TLR4 signal pathway may become a new direction for treating EMs.

Key words: Endometriosis , Inflammation, Stress reaction, Toll-like receptor 4;, TLR4 signal pathway