Bench-to-bedside review: acute respiratory distress syndrome - how neutrophils migrate into the lung.

Bench-to-bedside review: acute respiratory distress syndrome - how neutrophils migrate into the lung.
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DOI:
10.1186/cc2881
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发表时间:
2004-12
期刊:
Critical care (London, England)
影响因子:
--
通讯作者:
Ley K
Ley K
中科院分区:
其他
文献类型:
--
作者:
Reutershan J;Ley K

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急性肺损伤及其更严重的形式,急性呼吸窘迫综合征,是危重患者的主要挑战。循环中性粒细胞的激活和迁移到肺泡空气空间与急性肺损伤的发展相关,并且在许多实验模型中中性粒细胞募集的抑制剂减轻肺损伤。肺中中性粒细胞募集的分子机制与其他组织中的分子机制有根本的不同。不同的信号似乎调节中性粒细胞从血管内进入间质和肺泡室。进入肺泡室受CXC趋化因子受体(CXCR)2及其配体(CXC趋化因子配体[CXCL]1-8)的控制。控制中性粒细胞隔离进入肺血管室的机制涉及肌动蛋白细胞骨架和粘附分子的变化,包括选择素、β2整合素和细胞间粘附分子-1。中性粒细胞进入肺间质空间的机制目前尚不清楚。本文就中性粒细胞在炎症肺中的转运机制及其与肺损伤的关系作一综述。
Acute lung injury and its more severe form, acute respiratory distress syndrome, are major challenges in critically ill patients. Activation of circulating neutrophils and transmigration into the alveolar airspace are associated with development of acute lung injury, and inhibitors of neutrophil recruitment attenuate lung damage in many experimental models. The molecular mechanisms of neutrophil recruitment in the lung differ fundamentally from those in other tissues. Distinct signals appear to regulate neutrophil passage from the intravascular into the interstitial and alveolar compartments. Entry into the alveolar compartment is under the control of CXC chemokine receptor (CXCR)2 and its ligands (CXC chemokine ligand [CXCL]1–8). The mechanisms that govern neutrophil sequestration into the vascular compartment of the lung involve changes in the actin cytoskeleton and adhesion molecules, including selectins, β2 integrins and intercellular adhesion molecule-1. The mechanisms of neutrophil entry into the lung interstitial space are currently unknown. This review summarizes mechanisms of neutrophil trafficking in the inflamed lung and their relevance to lung injury.
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