Shao Lujing, Wang Chunxia, Zhang Yucai
Department of Critical Care Medicine, Shanghai Children's Hospital, Shanghai Jiao Tong University, Institute of Pediatric Critical Care, Shanghai Jiao Tong University, Shanghai 200062, China. Corresponding author: Zhang Yucai, Email:
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2019 Jul;31(7):910-912. doi: 10.3760/cma.j.issn.2095-4352.2019.07.023.
Immunosuppression plays a critical role in death of sepsis. Innate immunity is the first line defense to prevent pathogen invasion, and neutrophils, macrophages, dendritic cells and natural killer cells (NK cells) are closely involved in the process of the immune-regulation during sepsis. Recently, metabolic reprogramming in immune cells is known as a keystone for immune intervention therapy in sepsis. Here, we focus on the recent advances in metabolic regulation in neutrophils, macrophages, dendritic cells and NK cells including glycolysis, fatty acid synthesis, fatty acid oxidation and arginine metabolism involved in the immune-regulation of sepsis. This review will be helpful to summarize the mechanisms underlying sepsis-induced immunosuppression.
免疫抑制在脓毒症死亡中起关键作用。固有免疫是预防病原体入侵的第一道防线,中性粒细胞、巨噬细胞、树突状细胞和自然杀伤细胞(NK细胞)密切参与脓毒症期间的免疫调节过程。最近,免疫细胞中的代谢重编程被认为是脓毒症免疫干预治疗的关键。在此,我们聚焦于中性粒细胞、巨噬细胞、树突状细胞和NK细胞代谢调节的最新进展,包括参与脓毒症免疫调节的糖酵解、脂肪酸合成、脂肪酸氧化和精氨酸代谢。这篇综述将有助于总结脓毒症诱导免疫抑制的潜在机制。