Abstract
Purpose :
Ectoine is a bacteria-derived extremolyte with the ability to protect proteins and biological membranes from damage. The purpose of this study was to investigate protective effects of ectoine in preventing corneal epithelial barrier from disruption using a murine dry eye model induced by desiccating stress (DS)
Methods :
C57BL/6 mice were subjected to DS for 5 days, and topically treated with 2% ectoine or 10 ng/ml of rhIL-38, with PBS as vehicle control. Oregon-green-dextran (OGD) uptake was used to measure corneal defect and barrier function. And corneal tissues will be collected for whole cornea flat mount immunofluorescent staining to evaluate the barrier protein structure of tight junction proteins ZO-1 and occludin. Gene expression was detected by RT-qPCR.
Results :
Desiccating stress significantly stimulated expression of IL-36α by corneal epithelia and conjunctiva, and disrupted corneal barrier proteins tight junction ZO-1 and occludin in C57BL/6 mice, as evaluated by RT-qPCR and immunostaining. Compared to the vehicle group, topically treatment of DS mice with ectoine or a IL-36 receptor antagonist rhIL-38, largely relieved the clinical signs of ocular irritation and inflammation, reduced corneal permeability to OGD, restored barrier protein structure and integrity of ZO-1 and occludin, and decreased the expression of IL-36α.
Conclusions :
These findings suggest that ectoine, a bacteria-produced natural amino acid derivative, shows strong protective efficacy on ocular surface from inflammation and barrier disruption via suppressing IL-36α signaling pathway in the experimental dry eye model induced by desiccating stress.
This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.