Epithelium-Specific Ets-Like Transcription Factor 1, ESE-1, Regulates ICAM-1 Expression in Cultured Lung Epithelial Cell Lines

Abstract

Cystic fibrosis (CF) patients suffer from chronic airway inflammation with excessive neutrophil infiltration. Migration of neutrophils to the lung requires chemokine and cytokine signaling as well as cell adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1), which plays an important role in mediating adhesive interactions between effector and target cells in the immune system. In this study, we investigated the relationship betweenICAM-1and epithelium-specific ETS-like transcription factor 1 (ESE-1) and found thatICAM-1expression is upregulated in cell lines of CF (IB3-1) as well as non-CF (BEAS-2B and A549) epithelial origin in response to inflammatory cytokine stimulation. SinceESE-1is highly expressed in A549 cells without stimulation, we examined the effect ofESE-1knockdown onICAM-1expression in these cells. We found thatICAM-1expression was downregulated whenESE-1was knocked down in A549 cells. We also tested the effect ofESE-1knockdown on cell-cell interactions and demonstrate that the knocking downESE-1in A549 cells reduce their interactions with HL-60 cells (human promyelocytic leukemia cell line). These results suggest thatESE-1may play a role in regulating airway inflammation by regulatingICAM-1expression.