Fang Xiaohui, Matthay Michael A
Departments of Medicine and Anesthesia, Cardiovascular Research Institute, University of California, San Francisco, CA, USA.
Methods Mol Biol. 2018;1809:121-128. doi: 10.1007/978-1-4939-8570-8_10.
Alveolar epithelial barrier dysfunction contributes to the influx of protein-rich edema fluid and the accumulation of inflammatory cells in the pathogenesis of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). To study the alveolar epithelial barrier function under pathological conditions, we developed an in vitro model of acute lung injury using cultured human alveolar epithelial type II (ATII) cells. Here we describe the methods that we use to measure protein permeability and fluid transport across human ATII cell monolayers under stimulated conditions. Both proinflammatory cytokines and edema fluid from ALI/ARDS patients can increase protein permeability and decrease fluid transport across the human ATII cells monolayer.
肺泡上皮屏障功能障碍在急性肺损伤(ALI)和急性呼吸窘迫综合征(ARDS)的发病机制中,促使富含蛋白质的水肿液流入以及炎性细胞积聚。为研究病理条件下的肺泡上皮屏障功能,我们利用培养的人II型肺泡上皮(ATII)细胞建立了急性肺损伤的体外模型。在此,我们描述了在刺激条件下测量蛋白质通透性以及跨人ATII细胞单层的液体转运的方法。促炎细胞因子和ALI/ARDS患者的水肿液均可增加蛋白质通透性,并降低跨人ATII细胞单层的液体转运。