Pulmonary surfactant membranes (PSMs) function as a semipermeable membrane for O2/CO2 exchange and lowers the surface tension at the air/water interface preventing lungs from collapsing during the breathing cycle. PSMs respond to stress imposed by respiratory diseases. For instance, pneumonia alters the lipid composition of PSMs. However, a major missing link remains between the etiology of lung diseases and the fundamental properties of PSMs. To address this gap, we study PSMs in broncheoalveolar lavage samples collected from dolphins suffering from a range of respiratory diseases. Organic extractions isolate the lipidic phase, which upon re-hydration, organizes in diverse structures resembling native PSMs. Using X-rays, we found that lung pathology disrupts PSMs structure at two levels; severe lung disease leads to dehydration of PSM, and crystallization of their fatty acid chains. To assess the influence of disease on PSM film structure, we used AFM topography. We study the lateral distribution and interactions among the lipid phases, focusing specifically on the formation of liquid-condense LC domains, since these domains have been suggested to be important in surfactant function. We demonstrated that severity of illness affects LC domain size and shape, as well as surface coverage. Additionally, using AFM force spectroscopy, we report that severity of illness correlates with membrane loss of elasticity. Overall, this study links severity of lung pathology with the biophysical properties of pulmonary surfactant membranes providing new insights for respiratory therapies.

Lung pathology impairs pulmonary surfactant membrane physiology

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