Abstract：
BACKGROUND: Lung ischemia/reperfusion injury (LIRI) is a common occurrence in clinical practice and represents a significant complication following pulmonary transplantation and various diseases. At the core of pulmonary ischemia/reperfusion injury lies sterile inflammation, where the innate immune response plays a pivotal role. This review aims to investigate recent advancements in comprehending the role of innate immunity in LIRI.
METHODS: A computer-based online search was performed using the PubMed database and Web of Science database for published articles concerning lung ischemia/reperfusion injury, cell death, damage-associated molecular pattern molecules (DAMPs), innate immune cells, innate immunity, inflammation.
RESULTS: During the process of lung ischemia/reperfusion, cellular injury even death can occur. When cells are injured or undergo cell death, endogenous ligands known as DAMPs are released. These molecules can be recognized and bound by pattern recognition receptors (PRRs), leading to the recruitment and activation of innate immune cells. Subsequently, a cascade of inflammatory responses is triggered, ultimately exacerbating pulmonary injury. These steps are complex and interrelated rather than being in a linear relationship. In recent years, significant progress has been made in understanding the immunological mechanisms of LIRI, involving novel types of cell death, the ability of receptors other than PRRs to recognize DAMPs, and a more detailed mechanism of action of innate immune cells in ischemia/reperfusion injury (IRI), laying the groundwork for the development of novel diagnostic and therapeutic approaches.
CONCLUSIONS: Various immune components of the innate immune system play critical roles in lung injury after ischemia/reperfusion. Preventing cell death and the release of DAMPs, interrupting DAMPs receptor interactions, disrupting intracellular inflammatory signaling pathways, and minimizing immune cell recruitment are essential for lung protection in LIRI.
METHODS: A computer-based online search was performed using the PubMed database and Web of Science database for published articles concerning lung ischemia/reperfusion injury, cell death, damage-associated molecular pattern molecules (DAMPs), innate immune cells, innate immunity, inflammation.
RESULTS: During the process of lung ischemia/reperfusion, cellular injury even death can occur. When cells are injured or undergo cell death, endogenous ligands known as DAMPs are released. These molecules can be recognized and bound by pattern recognition receptors (PRRs), leading to the recruitment and activation of innate immune cells. Subsequently, a cascade of inflammatory responses is triggered, ultimately exacerbating pulmonary injury. These steps are complex and interrelated rather than being in a linear relationship. In recent years, significant progress has been made in understanding the immunological mechanisms of LIRI, involving novel types of cell death, the ability of receptors other than PRRs to recognize DAMPs, and a more detailed mechanism of action of innate immune cells in ischemia/reperfusion injury (IRI), laying the groundwork for the development of novel diagnostic and therapeutic approaches.
CONCLUSIONS: Various immune components of the innate immune system play critical roles in lung injury after ischemia/reperfusion. Preventing cell death and the release of DAMPs, interrupting DAMPs receptor interactions, disrupting intracellular inflammatory signaling pathways, and minimizing immune cell recruitment are essential for lung protection in LIRI.
摘要：
背景：肺缺血/再灌注损伤（LIRI）在临床实践中很常见，是肺移植和各种疾病后的重要并发症。肺缺血/再灌注损伤的核心在于无菌性炎症,先天免疫反应起着关键作用。这篇综述旨在探讨在理解先天免疫在LIRI中的作用方面的最新进展。
方法：使用PubMed数据库和WebofScience数据库进行了基于计算机的在线搜索，以获取有关肺缺血/再灌注损伤的已发表的文章，细胞死亡,损伤相关分子模式分子(DAMPs)，先天免疫细胞，先天免疫,炎症。
结果：在肺缺血/再灌注过程中，细胞损伤甚至死亡都可能发生。当细胞受伤或经历细胞死亡时，称为DAMPs的内源性配体被释放。这些分子可以被模式识别受体（PRR）识别和结合，导致先天免疫细胞的募集和激活。随后，引发一系列炎症反应，最终加重肺损伤。这些步骤是复杂且相互关联的，而不是线性关系。近年来,在了解LIRI的免疫机制方面取得了重大进展，涉及新类型的细胞死亡，PRR以外的受体识别DAMPs的能力，和更详细的作用机制的先天免疫细胞在缺血/再灌注损伤（IRI），为开发新的诊断和治疗方法奠定基础。
结论：先天性免疫系统的各种免疫成分在缺血/再灌注后的肺损伤中起关键作用。防止细胞死亡和DAMP的释放，中断DAMPs受体相互作用，破坏细胞内炎症信号通路，和最小化免疫细胞募集对于LIRI的肺保护至关重要。
方法：使用PubMed数据库和WebofScience数据库进行了基于计算机的在线搜索，以获取有关肺缺血/再灌注损伤的已发表的文章，细胞死亡,损伤相关分子模式分子(DAMPs)，先天免疫细胞，先天免疫,炎症。
结果：在肺缺血/再灌注过程中，细胞损伤甚至死亡都可能发生。当细胞受伤或经历细胞死亡时，称为DAMPs的内源性配体被释放。这些分子可以被模式识别受体（PRR）识别和结合，导致先天免疫细胞的募集和激活。随后，引发一系列炎症反应，最终加重肺损伤。这些步骤是复杂且相互关联的，而不是线性关系。近年来,在了解LIRI的免疫机制方面取得了重大进展，涉及新类型的细胞死亡，PRR以外的受体识别DAMPs的能力，和更详细的作用机制的先天免疫细胞在缺血/再灌注损伤（IRI），为开发新的诊断和治疗方法奠定基础。
结论：先天性免疫系统的各种免疫成分在缺血/再灌注后的肺损伤中起关键作用。防止细胞死亡和DAMP的释放，中断DAMPs受体相互作用，破坏细胞内炎症信号通路，和最小化免疫细胞募集对于LIRI的肺保护至关重要。
