Cytokine modulation of human corneal epithelial cell ICAM-1 (CD54) expression

To determine whether pro-inflammatory cytokines modulate intercellular adhesion molecule-1 (ICAM1; CD54) expression on cultured primary human corneal epithelial cells (HCEs), confluent HCEs were treated with various concentrations of interferon-γ (IFN-γ), interleukin-1α (IL-1α), IL-1β, IL-4, tumor necrosis factor-α (TNF-α), or combinations over time. ICAM-1 expression was measured by flow cytometry and/or a cell-based ELISA using a monoclonal mouse anti-human CD54 antibody. The apparent MW of ICAM-1 protein was determined by immunoprecipitation of biotinylated HCEs. RT-PCR was used to detect ICAM-1 RNA. The mature celt surface form of HCE ICAM-1 was ~ 110 kDa as determined by immunoprecipitation. IFN-γ and TNF-α induced both dose- and time-dependent increases in ICAM-1 expression. An ~ 20-fold increase in ICAM-1 was seen at 50-100 U IFN-γ ml^-1. ICAM-1 specific mRNA accumulated ~ 4.5-fold after IFN-γ treatment. TNF-α (100 U ml^-1) induced a consistent ~ 6.0-fold increase in ICAM-1 expression. When IFN-γ and TNF- α were mixed, at sub-optimal concentrations of each, a synergistic effect on ICAM-1 expression was not detected. Neither IL-4, IL-1α nor IL-1β affected ICAM-1 expression in a consistent fashion. In summary, ICAM-1 was modulated on primary human corneal epithelial cells by the cytokines IFN-γ and TNF-α in a dose- and time-dependent fashion. Cytokine modulation of corneal epithelial cell ICAM-1 during inflammation may contribute to corneal epithelial cell injury by aiding the attachment of inflammatory cells such as eosinophils which express the receptor for ICAM-1, the β₂ integrins (CD11a,b,c/CD18).