Abstract
Sjögren syndrome (SS) or dry eye disease (DED) is one of the most complicated ocular surface diseases. The goal of this study is to elucidate the relationship of the changes in clinical indices of tear film (TF) homeostasis with respect to tear components to allow for SS-DED monitoring and avoid stably controlled SS-DED patients from re-entering a vicious cycle. This prospective case-control study compared stable SS-DED patients with non-SS-DED control from several aspects, including clinical indices for TF homeostasis, 2 DED diagnostic biomarkers (MMP-9 and lactoferrin), and the proteome of flush tears. Compared with non-SS-DED controls, stably controlled SS-DED subjects had less tear secretion and higher ocular surface inflammation, a higher concentration ratio of tear MMP-9/lactoferrin, a more diverse tear proteome, and lower spectral intensities of lipocalin-1, lacritin, and prolactin-inducible protein among the abundant tear proteins. For stable SS-DED patients, the concentration ratio of tear MMP-9/lactoferrin and the corrected lipocalin-1 signal was positively correlated with ocular inflammation and TF stability, respectively. MMP-9 released from stressed ocular surface epithelium and lipocalin-1 secreted from the energetic lacrimal gland are two tear biomarkers responding well to TF homeostasis. The tear proteomics approach through flush tears is a promising method for monitoring SS-DED patients with a standardized sampling procedure and lactoferrin-corrected analysis.
Highlights
Dry eye disease (DED) is a distressing and even disabling disease that has been increasingly emphasized worldwide following its growing population [1]
We selected a set of tests, including three significant indices and two marginally significant indices (OSDI and NIKBUT first of tear break-up time (TBUT)) as clinical monitoring indices
We found lipocalin-1, lacritin, and prolactin-inducible protein were still significantly downregulated in stably controlled Sjögren syndrome (SS)-DED patients
Summary
Dry eye disease (DED) is a distressing and even disabling disease that has been increasingly emphasized worldwide following its growing population [1]. A loss of tear film homeostasis with ocular surface inflammation may be a response to changes in tear components. It is highly valuable to identify the change of tear components by responding to the cyclical process of DED from breakdown of tear film homeostasis to ocular surface inflammation. Understanding the change of clinical indices of tear film homeostasis by the altering tear components will be helpful for eye care practitioners to monitor the treatment of DED and prevent stably controlled DED patients from re-entering the vicious cycle. DED is more prevalent in patients with autoimmune diseases, which affect around 8% of the population, of whom 78% are women [3]. Exploring the association between tear film homeostasis and tear components of SS-DED is of utmost importance
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