The ocular tear film is composed of an aqueous and mucin layer covered by a lipid film. The total thickness of the tear film is about 10 μm, and the lipid layer is about 100 nm thick. The lipid layer of the ocular tear film provides a physical barrier against foreign bodies, lubricates the eyelid during blinking, lowers the surface tension of the tear film to facilitate spreading across the cornea, and reduces evaporation of the aqueous phase. In order to perform these functions, the lipid film must be continuously intact during the compression and expansion caused by blinking. The lipid layer is composed of 60-70% wax esters, cholesterol esters, and triglycerides. In a Langmuir trough, cholesterol myristate does not respread well after compression on a water subphase. Soluble proteins in the aqueous phase of the tear film are known to adsorb at the lipid-aqueous interface in vitro. The presence of absorbed or denatured protein in the lipid layer alters the surface tension of the interface and may facilitate spreading of the lipid layer. A deficiency in the production of protein, aqueous phase, or lipid or an increase in the rate of tear film evaporation leads to dry eye syndrome. In this work, the tear film is modeled using a simple lipid mixture, lysozyme, and a polymer. The effect of these tear film components on the ability of a thick lipid layer (100 nm) to wet an aqueous subphase is determined using surface tension measurements, Brewster angle microscopy and fluorescence microscopy. The interfacial shear rheology of the resulting model tear film interface is determined using the interfacial stress rheometer.