Normal respiration depends on the surface activity of endogenous pulmonary surfactant (PS) contained within the thin liquid layer lining the lungs. PS must adsorb rapidly to form a film that can reduce the surface tension to near zero-value when the film is compressed during expiration. Severe pulmonary disease results if this surfactant is deficient or if its activity is otherwise compromised.

The detection of phosphatidylglycerol (PG) is generally used as a marker of fetal lung maturity. In a model system, the presence of PG was shown to accelerate the initial stages of vesicle adsorption [1]. In the current study, the mechanisms by which electrostatic interactions rate-limit the adsorption of a model surfactant system to a clean air-water interface were investigated. Vesicles of the same approximate size distribution, as determined by dynamic light scattering, were formed from the zwitterionic lipid dioleoylphosphatidylcholine (DOPC), the anionic lipid dioleoylphosphatidylglycerol (DOPG), and mixtures thereof. The surface charge density of the vesicle, from fully uncharged to fully charged, was controlled by the variation of the vesicle composition.

The measured adsorption rates, as quantitated by the duration of the initial induction period in the dynamic surface tension response, were consistent with a model of an electrostatic barrier to vesicle adsorption: vesicles with a higher net surface charge adsorbed slower than those with a lower net charge, screening of the surface charge resulted in faster adsorption. The data are interpreted within the context of a simple mass transfer model that considers the disruption of the vesicle bilayer as the crucial step in the adsorption process. The characterization of a well-defined phospholipid model system is the first step in the elucidation of the mechanisms controlling the initial stages of PS adsorption.

[1] Walters, Jenq, and Hall, “Distinct Steps in the Adsorption of Pulmonary Surfactant to an Air-Liquid Interface,” Biophysical Journal 78:257, 2000