Hu Xiyou, Chen Bo, Chen Zelin
Research Center of Experimental Acupuncture Science, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China.
Department of Cardiovascular Diseases, The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang 550002, Guizhou, China.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2022 Jun;34(6):661-665. doi: 10.3760/cma.j.cn121430-20210701-00992.
Sepsis is a systemic reaction syndrome caused by various infectious factors,and its core mechanism is immue disorder. Macrophages, known as the most important component of innate immunity, play an important role in the occurrence and development of sepsis. Macrophage polarization has been shown to be closely related to inflammation and immunity. In the occurrence and development of sepsis,the mechanisms are complex and unclearly. The release of inflammatory factors and the occurrence of inflammatory responses will be regulated by changes in macrophage polarization phenotype. Multiple signaling pathways such as Toll-like receptor 4/nuclear transcription factor-κB (TLR4/NF-κB), phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt), Janus kinase/signal transduction and transcription activator (JAK/STAT), adenosine-activated protein kinase-peroxisome proliferation-activated receptor γ (AMPK-PPARγ), Notch, C-Jun amino terminal kinase (JNK), nuclear factor E2-related factor 2 (Nrf2), etc. are involved in the regulation of macrophage polarization,and interact with each other.Regulation of macrophage polarization will be a new target for the prevention and treatment of the occurrence, development and prognosis of sepsis. This paper summarized the latest progress of macrophage polarization phenotype in the occurrence and development of sepsis, aiming to provide new ideas and methods for clinical prevention and treatment of sepsis.
脓毒症是由各种感染因素引起的全身反应综合征,其核心机制是免疫紊乱。巨噬细胞作为天然免疫的最重要组成部分,在脓毒症的发生发展中起重要作用。巨噬细胞极化已被证明与炎症和免疫密切相关。在脓毒症的发生发展过程中,机制复杂且尚不清楚。炎症因子的释放和炎症反应的发生将受巨噬细胞极化表型变化的调控。Toll样受体4/核转录因子-κB(TLR4/NF-κB)、磷脂酰肌醇3激酶/蛋白激酶B(PI3K/Akt)、Janus激酶/信号转导及转录激活因子(JAK/STAT)、腺苷激活蛋白激酶-过氧化物酶体增殖物激活受体γ(AMPK-PPARγ)、Notch、C-Jun氨基末端激酶(JNK)、核因子E2相关因子2(Nrf2)等多条信号通路参与巨噬细胞极化的调控,且相互作用。调控巨噬细胞极化将成为脓毒症发生、发展及预后防治的新靶点。本文综述了巨噬细胞极化表型在脓毒症发生发展中的最新研究进展,旨在为脓毒症的临床防治提供新思路和方法。