(595i) Tug of War At the Air/Water Interface: The Role of Cholesterol and SP-B On Controlling the Line Tension of Model Lung Surfactants

Lung surfactant is a complex mixture of lipids and proteins that work to regulate the interfacial tension in the lung, minimizing the work of breathing as well as insuring uniform lung inflation. A lack or dysfunction of lung surfactant can result in various respiratory diseases, such as Neonatal Respiratory Distress Syndrome (NRDS), and Acute Respiratory Distress Syndrome (ARDS). In this study, we will present our research findings on (a) how small and elevated amounts of cholesterol control the adsorption and surface tension lowering properties of synthetic surfactant mixtures (b) how cholesterol-surfactant protein SP-B alter the morphology and energy of a model lung surfactant film. A langmuir trough coupled with a Wilhelmy plate pressure sensor has been used as an in vitro model to record the surface activity of our model surfactant mixtures at the air/water interface in the alveoli.  Using fluorescence microscopy, alterations in the domain morphology of lipid molecules is recorded as a function of cholesterol and SP-B content. The size distribution is then fitted with a theoretical model recently developed by us, that allows us to simultaneously monitor changes in the line tension l and dipole density difference m . Using this technique, we report that (a) individually Cholesterol and surfactant protein SP-B show opposing effects on the lateral organization of domains, (b) SP-B plays a more dominating role than cholesterol when modulating the line tension at the interface. This may well be because of electrostatic interactions between the negatively charged unsaturated lipids in our model surfactant and the positively charged protein.