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Nitya Kumar, John Awad, Mike de Jesus, Keri Smith, Mary McGuire, Richard W Yee, Sean Spector; Ocular Surface Cytokines after Computer-related Stress. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1859.
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Recent research has shown that chronic computer screen usage is a major risk factor for dry eye disorders, with inflammation considered to be a primary contributor. In this pilot study, we investigated acute changes in ocular surface inflammation as measured by cytokine secretion after 1-hour of computer use. We hypothesized that acute computer usage can contribute to dry eye and is a major risk factor in dry eye.
Five Individuals (n=5) underwent a 1-hr test period playing Tetris on a computer. Subjects were positioned on a chin rest to maintain a constant eye-screen distance. Tears were collected via Schirmer’s strips before and after the testing period and processed to extract proteins. Cytokines were measured via a 42-plex Multiplex MAP assay (Millipore) and analyzed using a Luminex 200. Final pg/ml concentrations were adjusted for total tear volume based on Schirmer’s strip measurements.
Forty-two cytokines were analyzed; 29 were detectable in the majority of the samples. Notably, inflammatory cytokine, TNF, was low or not detectable in the majority of samples. Chemokines, including IP-10, were increased in all subjects, indicating their early transcription response to a stimulus. 80% of subjects exhibited >70% change in cytokine levels of either IL-6, IL-1, or IP-10. 80% of subjects also exhibited < 20% change in cytokine levels of either IL-6, IL-1, or IP-10. Over the 1-hour test period, 2 of the 5 patients consistently showed increased cytokine secretion in response to the challenge, while 3/5 consistently decreased cytokine secretion.
A possible explanation for TNF’s absence is TNF inhibition during certain types of acute stress, such as exercise. Research by Pedersen et al found that during exercise, muscle fibers produce IL-6 via a TNF-independent pathway. IL-6 then stimulates production of other anti-inflammatory cytokines such as IL-1ra and IL-10, while inhibiting proinflammatory cytokine TNF- α. Our study may be confirming that certain types of acute stress, similar to exercise, lead to inhibition of TNF as part of a protective mechanism. An additional control study will be performed and results reported upon completion to further evaluate this hypothesis. Moreover, the variation and acute changes in cytokine levels over a 1-hour testing period suggest that inflammatory responses were present in all subjects and are indicative of unique compensatory mechanisms in response to computer usage.
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