Molecular evidence for the role of inflammation in dry eye disease

Abstract

Ocular surface inflammation is propagated by a complex series of molecular processes and has been implicated in the pathogenesis of dry eye disease (DED), either as a causal or a downstream effect of ocular surface disease. A state of hyperosmolarity elicits an acute immune response in DED, leading to subsequent activation of the adaptive immune response. This cascade incites dysregulation of the immune system, triggering a vicious cycle of events that causes damage to the ocular surface. Symptoms associated with these events include burning, irritation, redness, photophobia and blurred vision. The chronic nature of the disease process can cause permanent alterations to the ocular surface and adnexa. An increasing investment in treatment options, and positive outcomes with novel therapies that have received subsequent regulatory approval, lends further support to the role of inflammation in DED. This review highlights the nature and function of a range of fundamental inflammatory molecules in DED to provide the clinician with an appreciation for the ways in which these factors might be manipulated in DED management.

Chronic dry eye induced corneal hypersensitivity, neuroinflammatory responses, and synaptic plasticity in the mouse trigeminal brainstem

“…Ocular surface alterations and inflammation are the core mechanisms of DED [45, 46]. Here, we show that mice that underwent excision of the glands developed corneal surface alterations and inflammation by d7, which was maintained until d21 post-surgery.…”

Comparison of Two Experimental Mouse Dry Eye Models through Inflammatory Gene Set Enrichment Analysis Based on a Multiplexed Transcriptomic Approach

“…Over the past few decades, numerous research studies have described modulation of inflammatory mediators in the tear film or ocular surface tissues, supporting the hypothesis that inflammation is one of the core mechanisms of DED [ 4 , 5 , 6 , 7 , 8 ] ( Table 1 ).…”

The Application of Artificial Neural Networks and Logistic Regression in the Evaluation of Risk for Dry Eye after Vitrectomy

“…In addition, Banaee et al (2008) reported that scleral depression significantly increased risk for DED after vitrectomy [5]. e tear film, which comprises lipid, tear, and mucin layers, nourishes the conjunctival epithelium and cornea, supplies lubrication to facilitate opening and closing of the eyelids, and provides a high-quality optical surface for the cornea [13,14]. e pathogenesis of DED includes inflammation, apoptosis of the lacrimal gland cells and conjunctival epithelial cells, and androgen imbalance [13,14].…”