OBJECTIVE: In order to confirm the direct effect of glucocorticosteroids on epithelial intercellular adhesion molecule-1 (ICAM-1) expression, we examined ICAM-1 expression on primary cultured human nasal epithelial cells (HNECs) at both protein and mRNA levels. MATERIAL AND METHODS: HNECs were stimulated with recombinant human TNF-alpha (20 pg/mL-20 ng/mL) for specified time periods (0, 12, 24, and 48 h) and ICAM-1 mRNA and the soluble ICAM-1 (sICAM-1) concentrations were measured by quantitative RT-PCR and ELISA, respectively. We also evaluated surface expression of ICAM-1 by flow cytometry 48 h after stimulation and determined the effect of dexamethasone (DEX) on TNF-alpha-induced ICAM-1 expression. RESULTS: Significant increases in ICAM-1 gene expression in HNECs were initially detected at 24 h, peaking at 48 h after the stimulation. The TNF-mediated-ICAM-1 mRNA and ICAM-1 surface expression at 48 h was significantly inhibited by co-incubation with human recombinant soluble TNF receptor I. Similarly, TNF-alpha-induced release sICAM-1 occurred in a time- and concentration-dependent manner. DEX 10(-6) M attenuated the TNF-alpha-induced ICAM-1 expression at mRNA and protein levels. CONCLUSIONS: Our finding suggests a potential role for topical steroids in allergic rhinitis in suppressing inflammatory reactions in the nasal mucosa by regulating ICAM-1 expression on nasal epithelium.
OBJECTIVE: In order to confirm the direct effect of glucocorticosteroids on epithelial intercellular adhesion molecule-1 (ICAM-1) expression, we examined ICAM-1 expression on primary cultured human nasal epithelial cells (HNECs) at both protein and mRNA levels. MATERIAL AND METHODS: HNECs were stimulated with recombinant humanTNF-alpha (20 pg/mL-20 ng/mL) for specified time periods (0, 12, 24, and 48 h) and ICAM-1 mRNA and the soluble ICAM-1 (sICAM-1) concentrations were measured by quantitative RT-PCR and ELISA, respectively. We also evaluated surface expression of ICAM-1 by flow cytometry 48 h after stimulation and determined the effect of dexamethasone (DEX) on TNF-alpha-induced ICAM-1 expression. RESULTS: Significant increases in ICAM-1 gene expression in HNECs were initially detected at 24 h, peaking at 48 h after the stimulation. The TNF-mediated-ICAM-1 mRNA and ICAM-1 surface expression at 48 h was significantly inhibited by co-incubation with human recombinant soluble TNF receptor I. Similarly, TNF-alpha-induced release sICAM-1 occurred in a time- and concentration-dependent manner. DEX 10(-6) M attenuated the TNF-alpha-induced ICAM-1 expression at mRNA and protein levels. CONCLUSIONS: Our finding suggests a potential role for topical steroids in allergic rhinitis in suppressing inflammatory reactions in the nasal mucosa by regulating ICAM-1 expression on nasal epithelium.