The human tear film is essential for the protection of the corneal epithelium against drying and inflammation. The outermost layer at the aqueous air interface of the tear fluid lipid layer prevents the tear fluid from evaporation and decreases the surface tension at the interface. An increased evaporation rate of the tear fluid causes the dry eye syndrome (DES).
Molecules that are able to fluidize the lipid film might prevent the premature film rupture. A suitable molecule known to fluidize lipid films is ectoine, a compatible solute. We investigated the influence of ectoine on the structural organization of the natural and artificial tear fluid lipid layers using surface activity analysis and topographical studies. The natural meibomian lipids exhibit a continuous pressure-area isotherm without any phase transitions. In the presence of ectoine, the isotherm is expanded towards higher area per molecule implying decreased interaction between the lipid molecules. The AFM scans show presence of fiber like structures in the natural meibomian lipid film. In the presence of ectoine, droplet-like structures are observed which are hypothesized to be triacylglycerols excluded from the lipid film. In artificial tear films made of triacylglycerols, dipalmitoyl-phosphatidylcholine and cholestrol-palmitate, we observed the formation of similar drop-like structures in the presence of ectoine as in natural meibomian lipid films. Consequently, the hypothesis explaining the exclusion of tri/di acyl glycerol from the meibomian lipid film in the presence of ectoine in the subphase caused by the fluidizing effect of ectoine on meibomian lipid films is confirmed.