Analysing the potential anti-Inflammatory effects of vitamin D on human corneal epithelial cells

Inflammation of the ocular surface is required to remove a range of pathogens which come into contact with the anterior surface of the eye, lowering the risk of further pathological complications, such as diminished sight or blindness. The cornea is responsible for refracting light into the eye and must remain clear to ensure functionality. However, unregulated immune responses are associated with corneal tissue damage in a range of inflammatory ocular diseases, which manifests as a loss of visual capability. Previous studies have shown vitamin D metabolite 1,25-dihydroxyvitamin D3 (1,25D3) suppresses inflammatory pathways by modulating innate immune responses, including the production of pro-inflammatory mediators and antimicrobial peptides. This research used an in vitro model of corneal inflammation comprising of the human telomerase-immortalized corneal epithelial cell line (hTCEpi) together with various agonists to stimulate toll-like receptors (TLR) which are pattern recognition receptors. The TLR agonists produce inflammatory responses similar to the pathogens they represent. The effects of 10-7M 1,25D3 treatment on these responses were investigated. Using qRT-PCR, the study confirmed that 1,25D3 treatment significantly attenuated the expression of hTCEpi cell TLR3 (p