Interactions of Model Airborne Particulate Matter with Dipalmitoyl Phosphatidylcholine and a Clinical Surfactant Calsurf

Abstract Hypothesis Lung surfactant protects lung tissue and reduce 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. Experiments 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. Findings 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.