Nikitopoulou Ioanna, Ninou Ioanna, Manitsopoulos Nikolaos, Dimopoulou Ioanna, Orfanos Stylianos E, Aidinis Vassilis, Kotanidou Anastasia
1st Department of Critical Care Medicine & Pulmonary Services, GP Livanos and M Simou Laboratories, National and Kapodistrian University of Athens Medical School, Evangelismos Hospital, 45, Ipsilantou Street, Athens, Greece.
Institute of Immunology, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Intensive Care Med Exp. 2021 Mar 29;9(1):12. doi: 10.1186/s40635-021-00379-7.
The pathophysiology of acute respiratory distress syndrome (ARDS) may eventually result in heterogeneous lung collapse and edema-flooded airways, predisposing the lung to progressive tissue damage known as ventilator-induced lung injury (VILI). Autotaxin (ATX; ENPP2), the enzyme largely responsible for extracellular lysophosphatidic acid (LPA) production, has been suggested to play a pathogenic role in, among others, pulmonary inflammation and fibrosis.
C57BL/6 mice were subjected to low and high tidal volume mechanical ventilation using a small animal ventilator: respiratory mechanics were evaluated, and plasma and bronchoalveolar lavage fluid (BALF) samples were obtained. Total protein concentration was determined, and lung histopathology was further performed RESULTS: Injurious ventilation resulted in increased BALF levels of ATX. Genetic deletion of ATX from bronchial epithelial cells attenuated VILI-induced pulmonary edema.
ATX participates in VILI pathogenesis.
急性呼吸窘迫综合征（ARDS）的病理生理学最终可能导致肺组织不均匀塌陷以及气道被水肿液充斥，使肺易于发生进行性组织损伤，即呼吸机诱导的肺损伤（VILI）。自分泌运动因子（ATX；胞外核苷酸焦磷酸酶/磷酸二酯酶2）是主要负责细胞外溶血磷脂酸（LPA）生成的酶，有人认为它在肺部炎症和纤维化等过程中发挥致病作用。
使用小动物呼吸机对C57BL/6小鼠进行低潮气量和高潮气量机械通气：评估呼吸力学，并获取血浆和支气管肺泡灌洗液（BALF）样本。测定总蛋白浓度，并进一步进行肺组织病理学检查。结果：损伤性通气导致BALF中ATX水平升高。支气管上皮细胞中ATX的基因缺失减轻了VILI诱导的肺水肿。
ATX参与VILI的发病机制。
