Abstract
PurposeTo evaluate the ocular surface change and the inflammatory response in a rabbit model of short-term exposure keratopathy.MethodsShort term exposure keratopathy by continuous eyelid opening was induced in New Zealand white rabbits for up to 4 hours. Ultrasound pachymetry was used to detect central total corneal thickness. In vivo confocal microscopy and impression cytology were performed to evaluate the morphology of ocular surface epithelium and the infiltration of inflammatory cells. Immunohistochemistry for macrophage,neutrophil, CD4(+) T cells, and CD8(+) T cells were performed to classify the inflammatory cells. Scanning electron microscopy(SEM) was performed to detect ocular surface change.The concentrations of IL-8, IL-17, Line and TNF-αwere analyzed by multiplex immunobead assay. TUNEL staining was performed to detect cellular apoptosis.ResultsSignificant decrease ofcentral total cornealthickness were found within the first 5 minutes and remained stable thereafter, while there were no changes of corneal epithelial thickness.No significant change of corneal, limbal and conjunctival epithelial morphology was found by in vivo confocal microscopy except the time dependent increase of superficial cellular defects in the central cornea. Impression cytology also demonstrated time dependent increase of sloughing superficial cells of the central cornea. Aggregations ofinflammatory cells were found at 1 hour in the limbal epithelium, 2 hours in the perilimbal conjunctival epithelium, and 3 hours in the peripheral corneal epithelium.In eyes receiving exposure for 4 hours, the infiltration of the inflammatory cells can still be detected at 8 hours after closing eyes.Immunohistochemical study demonstrated the cells to be macrophages, neutrophils, CD4-T cells and CD-8 T cells.SEM demonstrated time-depending increase of intercellular border and sloughing of superficial epithelial cells in corneal surface. Time dependent increase of IL-8, IL-17 and TNF-α in tear was found.TUNEL staining revealed some apoptotic cells in the corneal epithelium and superficial stroma at 3 hours after exposure.ConclusionsShort term exposure keratopathy can cause significant changes to the ocular surface and inflammatory response. Decrease of central total corneal thickness, aggregation of inflammatory cells, and cornea epithelial cell and superficial keratocyte apoptosis were found no less than 4 hours following the insult.
Highlights
Significant decrease ofcentral total cornealthickness were found within the first 5 minutes and remained stable thereafter, while there were no changes of corneal epithelial thickness
Aggregations ofinflammatory cells were found at 1 hour in the limbal epithelium, 2 hours in the perilimbal conjunctival epithelium, and 3 hours in the peripheral corneal epithelium.In eyes receiving exposure for 4 hours, the infiltration of the inflammatory cells can still be detected at 8 hours after closing
Time dependent increase of IL-8, IL-17 and TNF-α in tear was found.transferase dUTP nick end labeling (TUNEL) staining revealed some apoptotic cells in the corneal epithelium and superficial stroma at 3 hours after exposure
Summary
The superficial part of the cornea is a layer of stratified, non-keratinized, non-secretory epithelium, whichrelies on a stable tear film to maintain healthy corneal physiology and optical properties.[1,2,3]Any pathological conditions causing dry eye disease may result in discomfort, visual impairment, and tear film instability with the potential to damage ocular surface.[4,5,6] Among the etiologies of dry eye syndrome, exposure keratopathy is uniquely caused by an unclosed eyelid, and incomplete blinking.[7,8,9,10]Eyelidclosure and blinking contribute to replenishing and spreading the tear film across the corneal surface and preventing tear film evaporation. The role of inflammation on the pathogenesis of aqueous tear deficientdry eyehas drawnresearch attention during the past few years, and anti-inflammatory agents have been proposed to treat dry eye syndrome in conjunction with the use of artificial tears.[37, 38]As for evaporative type of dry eye, most of the studies focusing on desiccating stress (with or without inhibition of tear secretion) in mouse eyes which were exposed to a controlled environment chamber with stable humidity and temperature In those studies, continuous desiccating stress was applied for about 10 hours a day for more than 1 week and the experimental mice can blink their eyes freely. Such experimental condition can be applied to patients with exposure keratopathy, especially for patients in intensive care units or operative rooms if the ocular surface is not adequately protected
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