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[天然免疫在通气诱导性肺损伤发病机制中的作用]

[Role of innate immunity in the pathogenesis of ventilation-induced lung injury].

作者信息

Shen Yi, Zhou Leilei, Jiang Wenqing, Zhang Xianming

机构信息

Department of Respiratory and Critical Medicine, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, Guizhou, China.

Department of Respiratory Medicine, Guizhou Second People's Hospital, Guiyang 550004, Guizhou, China. Corresponding author: Zhang Xianming, Email:

出版信息

Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2023 Apr;35(4):442-445. doi: 10.3760/cma.j.cn121430-20221012-00911.

DOI:10.3760/cma.j.cn121430-20221012-00911
PMID:37308205
Abstract

For patients receiving mechanical ventilation, mechanical ventilation is also an injury factor at the same time of treatment, which can lead to or aggravate lung injury, that is, ventilator-induced lung injury (VILI). The typical feature of VILI is that the mechanical stress is transmitted to cells through the pathway, leading to uncontrollable inflammatory cascade reaction, which causes the activation of inflammatory cells in the lung and the release of a large number of cytokines and inflammatory mediators. Among them, innate immunity is also involved in the occurrence and development of VILI. A large number of studies have shown that damaged lung tissue in VILI can regulate inflammatory response by releasing a large number of damage associated molecular pattern (DAMP). Pattern recognition receptor (PRR) participates in the activation of immune response by combining with DAMP, and releases a large number of inflammatory mediators to promote the occurrence and development of VILI. Recent studies have shown that inhibition of DAMP/PRR signaling pathway can play a protective role in VILI. Therefore, this article will mainly discuss the potential role of blocking DAMP/PRR signal pathway in VILI, and provide new ideas for the treatment of VILI.

摘要

对于接受机械通气的患者,机械通气在治疗的同时也是一种损伤因素,可导致或加重肺损伤,即呼吸机诱导的肺损伤(VILI)。VILI的典型特征是机械应力通过该途径传递至细胞,导致无法控制的炎症级联反应,进而引起肺内炎症细胞活化及大量细胞因子和炎症介质的释放。其中,固有免疫也参与了VILI的发生发展。大量研究表明,VILI中受损的肺组织可通过释放大量损伤相关分子模式(DAMP)来调节炎症反应。模式识别受体(PRR)通过与DAMP结合参与免疫反应的激活,并释放大量炎症介质以促进VILI的发生发展。近期研究表明,抑制DAMP/PRR信号通路可对VILI起到保护作用。因此,本文将主要探讨阻断DAMP/PRR信号通路在VILI中的潜在作用,为VILI的治疗提供新思路。

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