巨噬细胞极化在脓毒症发生发展中的作用

Role of macrophage polarization in the development of sepsis

脓毒症表现为炎症过度反应性疾病,主要由各种感染因素诱发,其核心机制为免疫障碍。被称为先天免疫中最重要组成部分的巨噬细胞,在脓毒症发生发展过程中发挥着重要作用。巨噬细胞极化已被证明与炎症和免疫力密切相关。脓毒症中巨噬细胞极化表型调节炎症因子的释放和炎症反应,其机制复杂,尚不完全清楚,多条信号通路如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/信号转导与转录激活因子(JAK/STAT)、腺苷酸活化蛋白激酶-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(Nrf 2)等参与巨噬细胞极化过程,各通路之间相互作用、相互影响。调节巨噬细胞极化将成为防治脓毒症发生发展、转归预后的新靶点。因此,本文对巨噬细胞极化表型在脓毒症发生发展过程中的最新进展进行总结,旨在为临床上脓毒症的防治提供新思路、新方法。

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 receptorγ(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.