Hane F T, Drolle E, Leonenko Z
Department of Biology, University of Waterloo, 200 University Ave, Waterloo, ON N2L 3G1, Canada.
Phys Chem Chem Phys. 2014 Aug 7;16(29):15430-6. doi: 10.1039/c4cp00040d.
A pulmonary surfactant (PS) is a thin lipid-protein film covering the surface of the lung alveoli at the air/liquid interface. The primary purpose of a PS is to control the surface tension of the air/liquid interface and to reduce the work of breathing. High levels of cholesterol in a PS are associated with life-threatening acute respiratory distress syndrome (ARDS) and acute lung injury (ALI). Finding therapeutics to counteract the effect of cholesterol in a PS is a matter of contemporary research. In our earlier work, we showed that the addition of amyloid-β (1-40) (Aβ40), the protein implicated in Alzheimer's disease, can reverse the detrimental effects of cholesterol in surfactants by improving multilayer formation and restoring PS surface active properties. We hypothesized that this phenomenon was due to Aβ40 improving adhesion properties of a surfactant. In this work we used atomic force spectroscopy to demonstrate that Aβ40 counteracts the adhesive properties of a PS compromised by high levels of cholesterol in a PS and helps to restore the functionality of a PS.
肺表面活性剂（PS）是一种位于气/液界面覆盖肺泡表面的薄脂质-蛋白质膜。PS的主要作用是控制气/液界面的表面张力并减少呼吸功。PS中高水平的胆固醇与危及生命的急性呼吸窘迫综合征（ARDS）和急性肺损伤（ALI）相关。寻找对抗PS中胆固醇作用的治疗方法是当代研究的一个课题。在我们早期的工作中，我们表明添加与阿尔茨海默病相关的淀粉样β蛋白（1-40）（Aβ40），可以通过改善多层结构形成和恢复PS表面活性特性来逆转胆固醇在表面活性剂中的有害作用。我们推测这种现象是由于Aβ40改善了表面活性剂的粘附特性。在这项工作中，我们使用原子力光谱法来证明Aβ40抵消了因PS中高水平胆固醇而受损的PS的粘附特性，并有助于恢复PS的功能。
