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Walter Nash, Alan Landers, Manal Gabriel, Jennifer Lane, Michael Foster; Secretory Phospholipase A2 Type IIA Levels across the Wear Cycle: Response to Lens Age or Indication of CL Intolerance. Invest. Ophthalmol. Vis. Sci. 2013;54(15):489.
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To evaluate the difference in day one versus day twenty-eight levels of secretory phospholipase A2 Type IIA (sPLA2IIA) in the tear envelope of symptomatic (decline in comfort over wear cycle) and asymptomatic subjects.
Lenses were collected from subjects aseptically and stored at below -20 degrees C. Subjects wore the same non-ionic silicone hydrogel lens material and used the same lens care regimen. Lenses were equilibrated to ambient temperature and rinsed in 2 mL of phosphate buffered saline for 5 minutes with agitation. The rinsate was subjected to a sandwich ELISA using a monoclonal antibody specific for sPLA2IIA. The plate was washed and an Acetylcholinesterase (ACHe); Fab’conjugate was added to the plate which selectively binds to a different epitope on the sPLA2IIA molecule. Finally, the enzymatic activity of ACHe was measured by adding a reagent containing the ACHe substrate and reading the plate at a wavelength of 420 nm by spectrophotometry.
Symptomatic and asymptomatic subjects exhibited similar levels of sPLA2IIA at day 1 as on day 28; with symptomatic subjects exhibiting 17.2±6.2 and 17.8±8.9 ng/lens sPLA2IIA, respectively, and asymptomatic subjects exhibiting 21.7±5.6 and 24.6±9.2 ng/lens sPLA2IIA, respectively. Comparing the amount sPLA2IIA in the tear envelope between symptomatic and asymptomatic subjects on both day 1 and day 28 showed no statistical differences using non-parametric Mann-Whitney analysis.
sPLA2IIA hydrolyzes fatty acids generating free arachidonic acid and lysophospholipids, the precursors of pro-inflammatory lipid mediators. Studies have reported elevated levels of sPLA2IIA in the tears of intolerant contact lens wearers. This study demonstrates no changes in the level of sPLA2IIA in the tear envelope over the course of the wear cycle in symptomatic or asymptomatic lens wearers. Our findings, suggest that the mechanism driving comfort at the time of lens replacement may not be the same as the mechanism driving contact lens intolerance as described in the literature.
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