Lung surfactant (LS), which is a complex mixture of lipids and proteins that line the epithelial surfaces of human and ther mammalian cells, has to achieve several seemingly contradictory features for proper lung function. First, LS must form a stable interfacial film with sufficient integrity to sustain high surface pressures (low surface tensions) on compression of the interface during exhalation and at the same time, it must spread quickly to re-cover the interface during inspiration. This requires a subtle balance of lipids and proteins in the interfacial films and may require different interfacial compositions and a wide variation in surface viscosity and elasticity during lung expansion and compression. A lack of LS in premature infants leads to neonatal respiratory distress syndrome (nRDS), which is treated by replacing the native LS with surfactants derived from animals. An important question in developing replacement surfactants is whether or not cholesterol belongs in a replacement lung surfactant and what the function of cholesterol could be, if it is indeed present at the interface.

We present detailed measurements of the macroscopic and microscopic surface viscosity of LS and phospholipid monolayers that show the two to three order of magnitude reduction in surface viscosity on addition of 1- 3 mole% cholesterol. This dramatic change in the ordering of the film is also seen in the monolayer compressibility and at slightly higher mole fractions, at the collapse pressure of the monolayers.

In addition, there is a crucial need for determining the viscoelastic properties of single lipid domains in multiphase monolayers to compare the local and global features of monolayer viscoelasticity. We will demonstrate, for the first time ever, an experimental setup which introduces microrheology and imaging to the field of biologically relevant monolayers and lung surfactants addressing single domains.