Role of innate immunity in the pathogenesis of ventilation-induced lung injury.
10.3760/cma.j.cn121430-20221012-00911
- Author:
Yi SHEN
1
;
Leilei ZHOU
1
;
Wenqing JIANG
2
;
Xianming ZHANG
1
Author Information
1. Department of Respiratory and Critical Medicine, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, Guizhou, China.
2. Department of Respiratory Medicine, Guizhou Second People's Hospital, Guiyang 550004, Guizhou, China. Corresponding author: Zhang Xianming, Email: 13078524367@163.com.
- Publication Type:Journal Article
- MeSH:
Humans;
Respiration, Artificial;
Respiration;
Immunity, Innate;
Ventilator-Induced Lung Injury;
Inflammation;
Inflammation Mediators;
Lung
- From:
Chinese Critical Care Medicine
2023;35(4):442-445
- CountryChina
- Language:Chinese
-
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.