Nrf2信号通路在复发性外阴阴道念珠菌病发病机制中的作用

摘要/Abstract

摘要：

复发性外阴阴道念珠菌病是一种由念珠菌机会感染引起的皮肤黏膜疾病，其发病机制复杂，而念珠菌的侵袭与宿主诱发因素是复发性外阴阴道念珠菌病的主要致病因素。其中，念珠菌可通过多种方式攻击宿主细胞和逃避宿主免疫系统而导致机体损伤。Nrf2信号通路是细胞抗氧化的主要调控机构，同时也是一种重要的免疫调节机构。一方面，Nrf2通路可下调NF-κB通路和促进Th17、Treg、Th1细胞的活化，启动宿主适应性免疫；同时，Nrf2通路可激活树突状细胞介导机体固有免疫。另一方面，Nrf2通路还可通过抗氧化应激损伤来阻止阴道炎的发展。该文对Nrf2通路在复发性念珠菌性阴道炎发病机制中的抗氧化应激和免疫调节作用进行综述，旨在研究Nrf2信号通路与复发性外阴阴道念珠菌病发病机制间的关系，从而指导临床治疗复发性外阴阴道念珠菌病。

关键词: 复发性外阴阴道念珠菌病, 免疫调节, Nrf2信号通路

Abstract:

Recurrent vulvovaginal candidiasis caused by Candida albicans had complex pathogenesis.The invasion of Candida albicans and host factors were the main pathogenic factors.Among them,Candida albicans could attack the host cells and evade the host immune system to hurt the body through various ways.The nuclear factor-E2-related factor 2 signaling pathway was not only a major regulator of cell oxidation,but also an important immune regulation mechanism.On the one hand,the activation of nuclear factor-E2-related factor 2 could initiat host adaptive immunity by inhibiting the expression of NF-κB to promot Th17、Treg and Th1 cells activation;at the same time,it also could activate dendritic cells to mediate the innate immune system.Besides,Nrf2 could prevent the development of vaginitis pathway through antioxidant stress.Here,we discussed the effects of Nrf2 signaling pathway on anti-oxidative stress and immunoregulation in the pathogenesis of recurrent vulvovaginal candidiasis,it aimed to investigate the relationship between Nrf2 signaling pathway and the pathogenesis of recurrent vulvovaginal candidiasis,so as to guide the clinic treatment of recurrent vulvovaginal candidiasis.

Key words: recurrent vulvovaginal candidosis, immune, Nrf2 signaling pathway

中图分类号:

R519.3

代歆悦, 莫子茵, 江娜, 高爱莉, 朱慧兰. Nrf2信号通路在复发性外阴阴道念珠菌病发病机制中的作用[J]. 中国真菌学杂志, 2017, 12(4): 240-243,232.

DAI Xin-yue, MO Zi-yin, JIANG Na, GAO Ai-li, ZHU Hui-lan. The pathogenesis of recurrent vulvovaginal candidiasis and the regulation of nuclear factor-E2-related factor 2 signaling pathway[J]. Chinese Journal of Mycology, 2017, 12(4): 240-243,232.

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