For a more detailed description of our recent research work, see discussion below or consult our list of recent publications.
Structure and stability of the tear film are among the key topics explored in our research group. This choice is relevant given that dysfunction of the tear film leads to the dry eye syndrome (DES) that is the most common eye disease affecting around 500 million people globally. Our research concentrates on understanding the tear film lipid layer (TFLL), which covers the tear film and decreases evaporation of the aqueous tear fluid. A dysfunctional TFLL is a key to understand the DES, since it causes excess evaporation and thereby drying of the ocular surface. Given these reasons, we combine experimental biophysics with computational simulations (see images below) to elucidate the nanoscale structure of the TFLL. This work has already revealed key mechanisms responsible for the evaporation-resistant properties of the TFLL.
Corneal epithelial health and stress response is one of our main interests, since it is also a key factor in development of dry eye syndrome: drying leads to tear fluid hyperosmolarity and consequent inflammation and damage to the corneal and conjunctival epithelium. In addition to the dry eye syndrome, corneal epithelium is also closely linked to our other clinical research topics (see below) carried out in the team. We use in vitro models of human corneal epithelial cells to study stress-induced pro-inflammatory responses (i.e. production and secretion of numerous chemokines and cytokines - IL-1, IL-8, TNFa as well as metalloproteinases) due to hyperosmolarity or drug toxicity. The pro-inflammatory profile significantly affects the viability of the cells at the ocular surface.
The group is involved in clinical research in a wide variety of topics, mostly focused on the anterior segment of the eye, such as refractive surgery, corneal infections and wound healing, peripheral hypertrophic subepithelial corneal degeneration, climatic droplet keratopathy, and ocular manifestations of hereditary gelsolin amyloidosis. For a more complete list, see our list of recent publications.