Dry eye disease (DED) is caused by inflammation and damage to the corneal surface due to tear film instability and hyperosmolarity. Various eye drops are used to treat this condition. Each eye drop has different properties and mechanisms of action, so the appropriate drug should be used according to clinical phenotypes. This study aims to compare the therapeutic mechanisms of cyclosporine A (CsA) and diquafosol tetrasodium (DQS). An experimental in vivo/in vitro model of DED using hyperosmolarity showed decreased cell viability, inhibited wound healing, and corneal damage compared to controls. Treatment with cyclosporine or diquafosol restored cell viability and wound healing and reduced corneal damage by hyperosmolarity. The expression of the inflammation-related genes il-1β, il-1α, and il-6 was reduced by cyclosporine and diquafosol, and the expression of Tnf-α, c1q, and il-17a was reduced by cyclosporine. Increased apoptosis in the DED model was confirmed by increased Bax and decreased Bcl-2 and Bcl-xl expression, but treatment with cyclosporine or diquafosol resulted in decreased apoptosis. Diquafosol increased NGF expression and translocation into the extracellular space. DED has different damage patterns depending on the progression of the lesion. Thus, depending on the type of lesion, eye drops should be selected according to the therapeutic target, focusing on repairing cellular damage when cellular repair is needed or reducing inflammation when inflammation is high and cellular damage is severe.

Steroid-induced cataracts (SIC) are defined as cataracts associated with the administration of corticosteroids. Long-term glucocorticoid treatment for inflammatory diseases reportedly increases the risk of SIC, and steroids can induce cataracts by disrupting ocular growth factor balance or homeostasis. In this study, we verified the effect of chondroitin sulfate proteoglycan 5 (CSPG5) using dexamethasone (dexa)-treated human lens epithelial (HLE-B3) cells and the lens epithelium from the anterior capsule of SIC patients obtained during cataract surgery. CSPG5 expression increased in the lens epithelium of SIC patients. The downregulation of CSPG5 suppressed the dexa-induced epithelial–mesenchymal transition (EMT)-related protein expression and motility in HLE-B3 cells. The disruption of the transcription factors EZH2 and B-Myb downregulated CSPG5, dexa-induced fibronectin expression, and cell migration in HLE-B3 cells, reaffirming that CSPG5 expression regulates EMT in lens epithelial cells. Taken together, these results indicate that the steroid-induced effects on lens epithelial cells are mediated via alterations in CSPG5 expression. Therefore, our study emphasizes the potential of CSPG5 as a therapeutic target for the prevention and treatment of SIC.

Dendritic cells are antigen-presenting cells that play essential roles in immunity and initiate immune reactions in experimental autoimmune encephalomyelitis (EAE) models. Dendritic cell recruitment was quantified in the optic nerve and retina after inducing the EAE model, and the correlation between functional and structural damage to the optic nerve and retina was determined. EAE was induced in female C57BL/6 mice by injecting murine myelin oligodendrocyte glycoprotein 35-55. All 20 mice were sacrificed sequentially. The dendritic cell infiltration level was analyzed using flow cytometry and immunofluorescence staining. Dendritic cell maturation-related factors were analyzed using quantitative PCR. The structural and functional in vivo readouts of each mouse were assessed using optical coherence tomography and optokinetic response, respectively. EAE induction increased inflammatory cell infiltration in the optic nerve and retina. The dendritic cell population was higher in the EAE group. The mRNA expression of factors associated with dendritic cell maturation was highly correlated with systemic and optic nerve functional damage. Dendritic cell infiltration and its maturation factors correlated with systemic neurologic deficits, optic nerve functional damage, and structural changes in the EAE model, accompanied by optic neuritis.