Invest Ophthalmol Vis Sci. 2009 Dec 3. [Epub ahead of print]
Glasgow BJ, Gasymov OK, Abduragimov AR, Engle JJ, Casey RC.
The Jules Stein Eye Institute - UCLA, Department of Ophthalmology, Los Angeles, United States.
Purpose: The cornea is protected by apical hydrophilic transmembrane mucins and tears. In pathologic states the mucin barrier is disrupted creating potential for meibomian lipids to adhere more strongly. Undisplaced lipids create an unwettable surface. The hypothesis that pathologic ocular surfaces alter lipid binding and the ability of tear proteins to remove lipids was tested. Methods: Corneas with pathologic surfaces were studied for lipid adhesion and removal by tears. Capture of fluorescent labeled phospholipids by human tears was assessed by steady state fluorometry. Tear proteins were separated by gel filtration chromatography and analyzed for bound lipids. Results: Contact angle measurements reveal strong lipid adherence to corneas submerged in buffer. Lower contact angles are observed for lipids on completely de-epithelialized versus intact corneas (p=0.04). Lipid removal from these surfaces is greater with whole tears than tears depleted of tear lipocalin (p<0.0005). Significantly less lipid is captured by tears from Bowman's layer than from epithelial bearing surfaces (p<0.025). The only tear component to bind the fluorescent tagged lipid is tear lipocalin. The histology of a rare case of dry eye disease demonstrates the dominant features of the contemporaneous bullous keratopathy. Lipid sequestration from this cornea by tear lipocalin was robust. Conclusions: Lipid is captured by tear lipocalin from corneas with bullous keratopathy and dry eye. Lipid removal is slightly abrogated by greater lipid adhesion to Bowman's layer. Reduced secretion of tear lipocalin documented in dry eye disease potentially could hamper lipid removal and exacerbate ocular surface pathology.
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