Monday, January 02, 2006

Role of Proteins in Dry Eye Disease
The homeostasis of the cornea is dependent on the proper interaction of the aqueous layer, mucins, lipids and corneal epithelial cells. The aqueous layer contains the proteins that have interaction with lipids and corneal epithelial cells. There is compelling evidence that one of these proteins called tear lipocalin has an important role in these interactions.
In tears of patients with meibomian gland dysfunction, both seborrheic and obstructive, the concentration of tear lipocalin is reduced (56). These conditions are associated with tear film instability and taken together raise the possibility that meibomian gland dysfunction coupled with decreased lipocalin could result in or worsen an abnormal ocular surface. Tear lipocalin is the principal lipid binding protein in tears (Glasgow 1995) and evidence is mounting that TL has a significant role in protection of the ocular surface from desiccation. Tear lipocalin scavenges lipid from the cornea to prevent dry spots from forming on the cornea. Lipids bound to tear lipocalin in aqueous provide a reservoir of lipid molecules in equilibrium with the surface and could reduce evaporation of water. The concentration of tear lipocalin as well as other protein components are decreased in dry eye disease (Janssen 2000). Furthermore, the concentration of tear lipocalin correlates with tear film stability in dry eye patients (Schoenwald 1997). The ocular surface is abnormal in dry eye disease. One of the objective criteria used widely for the diagnosis of dry eye is the presence of fluorescein staining of the cornea in areas where the epithelium has been disrupted (Nichols 2004). Punctate epithelial erosions occur in seborrheic blepharitis, a disease associated with aqueous tear deficiency. Epithelial erosions are quite common in forms of meibomian gland dysfunction (McCulley 1982). Tear lipocalin is reduced in both seborrheic blepharitis and meibomian gland dysfunction (Yamada 2005). Tear lipocalin has been shown to pick up lipids from the surface of the cornea, hence preventing the situation to occur where lipid on the cornea prevents the epithelium from becoming wettable.


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