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通过巨细胞代谢重编程介导的IL-10的抗炎作用

W K Eddie Ip¹, Namiko Hoshi¹, Dror S Shouval²

¹Department of Immunobiology and Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510, USA.

Science (New York, N.Y.)

|May 6, 2017

概括

通过促进氧化酸化和菌作用,防止了巨细胞的炎症代谢转变. 它的缺失导致线粒体受损,炎症酶激活,并在炎症条件下产生IL-1β.

科学领域:

免疫学
细胞代谢
线粒体生物学

背景情况:

互白素10 (IL-10) 是一种关键的抗炎细胞因子.
免疫细胞中的IL-10作用的确切机制尚未完全阐明.
炎症刺激会诱导巨细胞的新陈代谢程序.

研究的目的:

研究IL-10在炎症期间调节巨代谢重编程中的作用.
了解IL-10如何影响线粒体功能和线粒体衰变.
探索IL-10缺乏在炎症性疾病中的后果.

主要方法:

用脂聚糖 (LPS) 刺激的巨细胞培养
测量葡萄糖吸收,糖解和氧化酸化.
分析哺乳动物的拉皮素 (mTOR) 信号通路和DDIT4表达.
通过线粒体膜潜力和反应性氧物种 (ROS) 水平评估线粒体.
在大肠炎和患者样本的小鼠模型中评估NLRP3炎症酶激活和IL-1β产生.

主要成果:

IL-10抑制了LPS诱导的葡萄糖吸收和糖解,有利于氧化酸化.
通过诱导DDIT4,一种mTOR抑制剂,IL-10抑制了mTOR活性.
IL-10促进了线粒体,消除了功能障碍的线粒体.
缺少IL-10导致线粒体损伤的积累.
在大肠炎模型和IBD患者中,缺少IL-10信号导致NLRP3炎症酶激活和IL-1β产生.

结论:

IL-10积极反对巨细胞的炎症代谢重编程.
在维护线粒体质量控制方面,IL-10介导的线粒体吸食至关重要.
由于IL-10缺乏而导致的线粒体代谢功能障碍和线粒体衰竭导致IBD中的NLRP3炎症激活和炎症.

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