矿物皮醇通过ILC3s的受体依赖IL17的产生促进肠道炎症
Rongchuan Zhao1, Lei Hong2, Guohua Shi3
1School of Biomedical Engineering (Suzhou), Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230006, China; Suzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Science, Suzhou 215163, China.
阿尔多及其受体 (MR) 通过促进IL17在ILC3s中的作用,使炎症性肠病恶化. 用eplerenone阻断MR可以防止结肠炎,这表明了新的治疗策略.
科学领域:
- 免疫学 免疫学 免疫学
- 内分泌学 在内分泌学.
- 胃肠病学 胃肠病学
背景情况:
- 阿尔多斯特调节电解质和体积平衡.
- 矿物甲基皮质受体 (MR) 激活与炎症期间的免疫反应有关.
- 阿尔多斯特和MR在炎症性肠病 (IBD) 中的作用需要进一步研究.
研究的目的:
- 调查阿尔多斯和MR在IBD中的作用.
- 探索MR对抗性结肠炎的治疗潜力.
主要方法:
- 使用了DSS诱导的大肠炎小鼠模型.
- 评估了3组先天性淋巴细胞 (ILC3) 中的阿尔多斯特水平,IL17产生和ROS/RNS水平.
- 研究了在ILC3s.中对eplerenone (MR抗剂) 和Nr3c2 (MR基因) 缺陷的影响.
主要成果:
- 在结肠炎期间,结肠中阿尔多的水平升高.
- 阿尔多激素增加了IL17的产生和ILC3s中的ROS/RNS水平,加剧了肠道损伤.
- 埃普莱伦治疗和ILC3特异性MR缺乏症缓解了结肠炎,并降低了IL17和ROS/RNS的产生.
- MR直接与IL17A促进体结合,增强其转录.
结论:
- ILC3s中的阿尔多-MR-IL17信号在肠道平衡和IBD病变发生过程中起着至关重要的作用.
- 特别是与eplerenone的MR对抗,显示IBD的治疗潜力.
- 针对这种途径可以为IBD治疗提供一种新的策略.
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