Ocular surface inflammation

Although there are available therapies for acute-moderate ocular surface diseases, there is a lack of effective therapy for the treatment of more chronic-severe inflammatory diseases. These chronic-severe diseases are characterized for the possibility of corneal damage, that may lead to a sight-threatening outcome.

It is clear that secreted molecules from inflammatory cells are responsible for many of the features observed in ocular inflammatory diseases. However, there is growing evidence showing that epithelial cells are active participants in inflammation, as they express and produce a large number of molecules implicated in the initiation and perpetuation of the inflammation process. For that reason, epithelial cells, and in our case corneal epithelial cells, are considered as a potential target for therapeutic interventions.

This experimental model represents an in vitro model of ocular inflammation for the study of the implication of the corneal epithelium in the development of chronic-severe inflammatory diseases that may lead to visual loss.

In this model, the ocular surface cell lines have been exposed to different cytokines, including Th1 (INF-γ), Th2 (IL-4, IL-13) and Th17 (IL-17), and to TNF-α and TGF-β. Cell response in terms of cytokine/chemokine secretion and/or several receptor types’ expression has been characterized and the effect of several compounds (potential therapies) has been tested.