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1. Background and purpose

Upon eyelid opening after a blink, tear film (TF) is in a non-equilibrium state and undergoes a complex structural evolution. 1 In the final stages of this development, the film loses its continuity, which results in so called tear film breakup (TFBU). This phenomenon is critical because it leads to deterioration of the protective role of TF. Importantly, in dry eye disease (DED) the TFBU time is typically shortened according to different patterns, demonstrating that the disease is related to reduced TF stability. 2, 3 The aqueous tear layer at the corneal surface is stabilized by the presence of a relatively thin layer of lipids at the water-air interface, the so-called tear film lipid layer (TFLL). 4 It has been demonstrated that DED is accompanied by an alteration in TFLL composition, and that TFBU time depends on the properties of TFLL.

Even though TF deterioration and breakup are of key importance for understanding DED, neither the breakup mechanism nor the role played by lipids are understood at a very basic level; such an understanding is required for developing new DED treatments. For instance, it was observed that exogenous and relatively simple surfactant molecules, such as cetalkonium chloride (CKC), are able to stabilize TF in DED in mice and humans. 5, 6 Hence, it would be beneficial to understand the role of natural lipids in TFLL as well as the interactions between its endo-and exogenous components. We hypothesize that various lipid classes of TFLL play