Variation in the expression of inflammatory markers and neuroreceptors in human conjunctival epithelial cells.

The purpose of this research was to investigate the role of neurogenic involvement in the etiopatho-genesis of ocular surface inflammation, with the final goal of identifying new potential anti-inflammatory agents. We describe the presence of two "classic" markers of inflammation (HLA-DR and ICAM-1) and some neuroreceptors in cultured human conjunctival epithelial cells under basal and pro-inflammatory conditions. Two markers of inflammation (HLA-DR, ICAM-1) and several neuroreceptor subtypes (M1-, M2-, and M3-muscarinic; alpha1A-, alpha1B-, alpha1D-, alpha2A-, alpha2B-, alpha2C-, beta1-, beta2-, and beta3-adrenergic) were analyzed in a normal human conjunctival epithelial cell line (IOBA-NHC). These markers were studied in basal conditions and under the influence of two pro-inflammatory cytokines: tumor necrosis factor alpha (TNF-alpha) and/or interferon gamma (IFN-gamma). Immunofluorescence (confocal microscopy), western blotting, or flow cytometry techniques were used. In basal conditions, epithelial cells expressed all inflammatory markers except HLA-DR. The addition of IFN-gamma enhanced expression of HLA-DR, ICAM-1, and M2-muscarinic receptor. TNF-alpha up-regulated the expression of ICAM-1. When epithelial cells were incubated in the presence of both cytokines together, the cell surface expression of HLA-DR, ICAM-1, alpha1B-, and alpha2B-adrenergic receptors was increased. Cultured human conjunctival epithelial cells have been shown to be susceptible to up-regulation of the expression of inflammatory markers and cell membrane expression of some neuroreceptors under pro-inflammatory conditions. Consequently, pharmacologic neuro-modulation could have a role in the comprehensive management of ocular surface inflammation.