脓毒症发病机制复杂，涉及单核/巨噬细胞介导的固有免疫反应，而巨噬细胞功能的维持和改变与其代谢途径变化息息相关。正常生理条件下，巨噬细胞是以葡萄糖氧化磷酸化作为能量需求的主要代谢途径，其中M1型巨噬细胞表现为葡萄糖摄取与无氧糖酵解增加；M2型巨噬细胞则表现为脂肪酸摄取增加，氧化磷酸化效率提高。目前研究发现，缺氧诱导因子-1α、琥珀酸盐及谷氨酰胺等可能通过调控巨噬细胞代谢模式进而影响其功能。关注巨噬细胞代谢变化及代谢调节在脓毒症免疫发病机制中的作用，可能使巨噬细胞免疫代谢的靶点成为未来脓毒症治疗的突破口。“,”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.