Eyes that can’t properly clear away the debris of dead cells—known as defective autophagy—have been associated with inflammation and ocular surface disease. Knowing this, researchers explored the protective role trehalose may play in inflammation and desiccation-triggered stress in human corneal cells in vitro and in dry eye patients.
They found that trehalose reduces stress-induced inflammation through kinase inhibition and autophagy activation, and that topical administration of trehalose ameliorates dry eye-associated symptoms and reduces tear cytokine levels.
The team enrolled nine dry eye patients and administered trehalose in one eye and carboxymethylcellulose (CMC) in the other twice a day for 30 days. They evaluated OSDI scores, tear break-up times, Schirmer's test results and tear cytokine levels pre- and post-treatment. They then analyzed TNF-α and desiccation stress-induced human corneal cells with or without trehalose treatment for the expression levels of inflammatory- and autophagy-related markers.
The study authors discovered that cells treated with trehalose exhibited increased levels of autophagy markers compared with untreated cells. Trehalose also reduced cytokine levels in corneal cells experiencing stress-mediated inflammation. They add that topical administration of trehalose alleviated the clinical symptoms and tear cytokine levels in dry eye patients compared with CMC patients.
|1. Panigrahi T, Shivakumar S, Shetty R, et al. Trehalose augments autophagy to mitigate stress-induced inflammation in human corneal cells. Ocul Surf. August 11, 2019. [Epub ahead of print].|