Hypothesis: 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 (PM), 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 PM 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 PM was studied using isothermal titration calorimetry.
Findings: PM induced the expansion of the monolayers at low surface pressure (п) and film condensation at high п. Aggregation of PM mainly occurred at the interface of liquid expanded/liquid condensed (LE/LC) phases. PM 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 PM through complex binding modes attributed to the heterogeneity and amphiphilic property of PM This study improves the fundamental understanding of PM-lung surfactant interaction and shows useful implications of the toxicity of PM through respiration process.
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http://dx.doi.org/10.1016/j.jcis.2021.09.193 | DOI Listing |
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