出血性休克引发的肺中性粒细胞浸润的Toll样受体相互作用机制
TLR Cross-Talk Mechanism of Hemorrhagic Shock-Primed Pulmonary Neutrophil Infiltration.
作者信息
Fan Jie
机构信息
Department of Surgery, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA.
出版信息
Open Crit Care Med J. 2010 Jan 1;2:1-8. doi: 10.2174/1874828700902010001.
Abstract
Hemorrhage resulted from severe trauma renders patients susceptible to the development of acute lung injury (ALI). The accumulation of polymorphonuclear neutrophils (PMN) in the lung is a critical event in the development of ALI. PMN migration is a result of a cascade of cellular events, in which PMN, endothelial cells (EC), and macrophages (Mϕ) act in concert. Recent studies explored interrelated novel findings indicating that Toll-like receptors (TLRs) cross-talk mechanisms occurring in PMN, EC, and Mϕ are important determinants for hemorrhage-primed PMN migration. In Mϕ and EC, LPS acts through TLR4 signaling to up-regulate TLR2. Oxidant signaling derived from hemorrhage-activated PMN NAD(P)H oxidase enhances the TLR2 upregulation through PMN-Mϕ or PMN-EC interaction, resulting in an amplified release of cytokines and chemokines from the Mϕ and expression of adhesion molecules in the EC in response to TLR2 ligands, thereby promoting PMN migration. This review provides an insight of the mechanisms.
摘要
严重创伤导致的出血使患者易发生急性肺损伤（ALI）。肺内多形核中性粒细胞（PMN）的积聚是ALI发生过程中的关键事件。PMN迁移是一系列细胞事件的结果，其中PMN、内皮细胞（EC）和巨噬细胞（Mϕ）协同作用。最近的研究探索了相关的新发现，表明在PMN、EC和Mϕ中发生的Toll样受体（TLR）相互作用机制是出血引发的PMN迁移的重要决定因素。在Mϕ和EC中，脂多糖（LPS）通过TLR4信号传导来上调TLR2。出血激活的PMN烟酰胺腺嘌呤二核苷酸磷酸（NAD(P)H）氧化酶产生的氧化信号通过PMN-Mϕ或PMN-EC相互作用增强TLR2的上调，导致Mϕ中细胞因子和趋化因子的释放增加以及EC中黏附分子响应TLR2配体的表达，从而促进PMN迁移。本综述对这些机制进行了深入探讨。
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本文引用的文献
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