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Toll样受体诱导巨噬细胞脂质组重编程
作者:小柯机器人 发布时间:2020/6/9 14:56:45

美国加州大学洛杉矶分校Steven J. Bensinger小组的一项最新研究表明,Toll样受体诱导巨噬细胞脂质组重编程。相关论文于2020年6月8日在线发表在《细胞—代谢》杂志上。

研究人员使用互补的“ shotgun”和同位素示踪质谱方法来定义了由各种Toll样受体(TLR)和炎性细胞因子诱导的脂质生物合成、摄入和巨噬细胞组成的变化。“ shotgun”脂质组学数据显示,不同的TLR和细胞因子诱导巨噬细胞获得不同的脂质组,这表明它们在重塑脂质组成中具有特异性。机理研究表明,脂质组成的差异重编程是由MyD88和TRIF干扰素信号通路的相反作用所介导的。

最后,研究人员发现,干扰脂质成分的重编程可以增强炎症并促进宿主防御细菌攻击。这些研究为理解炎症刺激如何重编程巨噬细胞的脂质组成提供了框架,同时提供了利用差异脂质组学来影响免疫力的平台。

据了解,巨噬细胞响应激活信号重新编程其脂质代谢。但是,人们缺乏对不同促炎刺激物如何重塑巨噬细胞脂质组的系统性了解。

附:英文原文

Title: Toll-Like Receptors Induce Signal-Specific Reprogramming of the Macrophage Lipidome

Author: Wei-Yuan Hsieh, Quan D. Zhou, Autumn G. York, Kevin J. Williams, Philip O. Scumpia, Eliza B. Kronenberger, Xen Ping Hoi, Baolong Su, Xun Chi, Viet L. Bui, Elvira Khialeeva, Amber Kaplan, Young Min Son, Ajit S. Divakaruni, Jie Sun, Stephen T. Smale, Richard A. Flavell, Steven J. Bensinger

Issue&Volume: 2020-06-08

Abstract: Macrophages reprogram their lipid metabolism in response to activation signals. However,a systems-level understanding of how different pro-inflammatory stimuli reshape themacrophage lipidome is lacking. Here, we use complementary “shotgun” and isotope tracermass spectrometry approaches to define the changes in lipid biosynthesis, import,and composition of macrophages induced by various Toll-like receptors (TLRs) and inflammatorycytokines. “Shotgun” lipidomics data revealed that different TLRs and cytokines inducemacrophages to acquire distinct lipidomes, indicating their specificity in reshapinglipid composition. Mechanistic studies showed that differential reprogramming of lipidcomposition is mediated by the opposing effects of MyD88- and TRIF-interferon-signalingpathways. Finally, we applied these insights to show that perturbing reprogrammingof lipid composition can enhance inflammation and promote host defense to bacterialchallenge. These studies provide a framework for understanding how inflammatory stimulireprogram lipid composition of macrophages while providing a knowledge platform toexploit differential lipidomics to influence immunity.

DOI: 10.1016/j.cmet.2020.05.003

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(20)30242-4

期刊信息

Cell Metabolism:《细胞—代谢》,创刊于2005年。隶属于细胞出版社,最新IF:22.415
官方网址:https://www.cell.com/cell-metabolism/home
投稿链接:https://www.editorialmanager.com/cell-metabolism/default.aspx