Lung surfactant (LS) is a lipid-protein mixture that forms a monolayer that lines the alveolar air-liquid interface and acts to reduce the interfacial tension to a level necessary for breathing. The lack or inhibition of LS can be life threatening and can result in acute respiratory distress syndrome (ARDS) which has a 40% mortality rate. In prior work, we have shown that the LC phase domains of model lung surfactant monolayers of dipalmitoylphosphatidylcholine (DPPC), 1-hexadecanol (HD), and small (0.5 – 4 mol%) fractions of dihydrocholesterol (DChol) reversibly evolve from a circle morphology through a fingering instability to a uniform width stripe morphology. We hypothesized that the transition is due to a competition between intradomain electrostatic repulsion and interdomain line tension and these competing interactions set the stripe width. We also hypothesize that DPPC and HD co-crystallize at a fixed molar ratio in the LC domains, and that DChol preferentially localizes at the LE-LC interface, lowering the line tension. To examine these hypotheses, we transfer the monolayers from the air-water interface to mica substrates. We use Atomic Force Microscopy to optimize the monolayer transfer to show that a new inverted Langmuir-Schaefer method is superior to the established Langmuir-Blodgett deposition in preserving both LE and LC domain morphologies. We present an investigation of the nanomechanical properties using multimodal AFM including force volume, high-speed force-distance mapping, quantitative phase imaging, and friction force imaging. The electrostatic properties are probed via interleave-based Kelvin probe microscopy and chemical mapping via AFM infrared spectroscopy (AFM-IR) to investigate composition variations in the LC domains and LE matrix.

Nanomechanical mapping of phospholipid-cholesterol monolayers

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ACS Fall 2022

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