Xiao Xiao, Zhou Li, Xu Yan, Jiang Chunling
Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu 610041, Sichuan, China. Corresponding author: Jiang Chunling, Email:
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2020 Feb;32(2):249-252. doi: 10.3760/cma.j.cn121430-20191021-00049.
Immunopathogenesis of sepsis is a very complex process involving the innate immune responses mediated by mononuclear macrophages. However, the maintenance and change of macrophage function is closely associated with their immunometabolism. Macrophages take glucose oxidative phosphorylation as the main metabolic pathway under normal physiological conditions, M1 macrophages increase glucose uptake and anaerobic glycolysis, while M2 macrophages increase fatty acid uptake and oxidative phosphorylation efficiency. Recent findings showed that hypoxia-inducible factor-1α, succinate and glutamine were involved in macrophage function and metabolism regulation. Focusing on macrophages function and their immunometabolism changes in the immunopathogenesis of sepsis will make it possible to target immunometabolism as a breakthrough in the future therapy of sepsis.
脓毒症的免疫发病机制是一个非常复杂的过程，涉及单核巨噬细胞介导的固有免疫反应。然而，巨噬细胞功能的维持和变化与其免疫代谢密切相关。在正常生理条件下，巨噬细胞以葡萄糖氧化磷酸化为主要代谢途径，M1巨噬细胞增加葡萄糖摄取和无氧糖酵解，而M2巨噬细胞增加脂肪酸摄取和氧化磷酸化效率。最近的研究发现，缺氧诱导因子-1α、琥珀酸和谷氨酰胺参与巨噬细胞功能和代谢调节。关注巨噬细胞在脓毒症免疫发病机制中的功能及其免疫代谢变化，将使以免疫代谢为靶点成为未来脓毒症治疗的突破点。
