Abstract：
OBJECTIVE: Lung surfactant protects lung tissue and reduces the surface tension in the alveoli during respiration. Particulate matter with an aerodynamic diameter of less than 2.5 μm (PM2.5), which invades primely through inhalation, can deposit on and interact with the surfactant layer, leading to changes in the biophysical and morphological properties of the lung surfactant.
METHODS: Langmuir monolayers of 1,2-dipalmitoyl-sn-glycero-3-phosphatidylcholine (DPPC) and clinical surfactant Calsurf were investigated with a PM2.5 model injected into the water subphase, which were characterized by surface pressure-area isotherms, Brewster angle microscopy, atomic force microscopy, fluorescent microscopy, and x-ray photoelectron spectroscopy. The binding between DPPC/Calsurf and PM2.5 was studied using isothermal titration calorimetry.
RESULTS: PM2.5 induced the expansion of the monolayers at low surface pressure (п) and film condensation at high п. Aggregation of PM2.5 mainly occurred at the interface of liquid expanded/liquid condensed (LE/LC) phases. PM2.5 led to slimmer and ramified LC domains on DPPC and the reduction of nano-sized condensed domains on Calsurf. Both DPPC and Calsurf showed fast binding with PM2.5 through complex binding modes attributed to the heterogeneity and amphiphilic property of PM2.5. This study improves the fundamental understanding of PM2.5-lung surfactant interaction and shows useful implications of the toxicity of PM2.5 through respiration process.
METHODS: Langmuir monolayers of 1,2-dipalmitoyl-sn-glycero-3-phosphatidylcholine (DPPC) and clinical surfactant Calsurf were investigated with a PM2.5 model injected into the water subphase, which were characterized by surface pressure-area isotherms, Brewster angle microscopy, atomic force microscopy, fluorescent microscopy, and x-ray photoelectron spectroscopy. The binding between DPPC/Calsurf and PM2.5 was studied using isothermal titration calorimetry.
RESULTS: PM2.5 induced the expansion of the monolayers at low surface pressure (п) and film condensation at high п. Aggregation of PM2.5 mainly occurred at the interface of liquid expanded/liquid condensed (LE/LC) phases. PM2.5 led to slimmer and ramified LC domains on DPPC and the reduction of nano-sized condensed domains on Calsurf. Both DPPC and Calsurf showed fast binding with PM2.5 through complex binding modes attributed to the heterogeneity and amphiphilic property of PM2.5. This study improves the fundamental understanding of PM2.5-lung surfactant interaction and shows useful implications of the toxicity of PM2.5 through respiration process.
摘要：
目的：肺表面活性物质保护肺组织并降低呼吸过程中肺泡的表面张力。空气动力学直径小于2.5μm的颗粒物（PM2.5），主要是通过吸入侵入，可以沉积在表面活性剂层上并与之相互作用，导致肺表面活性剂的生物物理和形态特性发生变化。
方法：将1,2-二棕榈酰-sn-甘油-3-磷脂酰胆碱（DPPC）和临床表面活性剂Calsurf的Langmuir单层膜注入到水亚相中，以表面压力-面积等温线为特征，布鲁斯特角显微镜,原子力显微镜,荧光显微镜,和X射线光电子能谱。使用等温滴定量热法研究了DPPC/Calsurf与PM2.5之间的结合。
结果：PM2.5在低表面压力（Λ）下引起单层膨胀，在高Λ下引起薄膜凝结。PM2.5的聚集主要发生在液体膨胀/液体冷凝（LE/LC）相的界面处。PM2.5导致DPPC上的LC域变细和分枝化，并减少了Calsurf上的纳米级凝聚域。DPPC和Calsurf均通过复杂的结合模式与PM2.5快速结合，归因于PM2.5的异质性和两亲性。这项研究提高了对PM2.5-肺表面活性物质相互作用的基本理解，并显示了PM2.5通过呼吸过程的毒性的有用含义。
方法：将1,2-二棕榈酰-sn-甘油-3-磷脂酰胆碱（DPPC）和临床表面活性剂Calsurf的Langmuir单层膜注入到水亚相中，以表面压力-面积等温线为特征，布鲁斯特角显微镜,原子力显微镜,荧光显微镜,和X射线光电子能谱。使用等温滴定量热法研究了DPPC/Calsurf与PM2.5之间的结合。
结果：PM2.5在低表面压力（Λ）下引起单层膨胀，在高Λ下引起薄膜凝结。PM2.5的聚集主要发生在液体膨胀/液体冷凝（LE/LC）相的界面处。PM2.5导致DPPC上的LC域变细和分枝化，并减少了Calsurf上的纳米级凝聚域。DPPC和Calsurf均通过复杂的结合模式与PM2.5快速结合，归因于PM2.5的异质性和两亲性。这项研究提高了对PM2.5-肺表面活性物质相互作用的基本理解，并显示了PM2.5通过呼吸过程的毒性的有用含义。
