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Effect of glucocorticosteroids on tumour necrosis factor‐α‐induced intercellular adhesion molecule‐1 expression in cultured primary human nasal epithelial cells
Author(s) -
Shirasaki H.,
Watanabe K.,
Kanaizumi E.,
Sato J.,
Konno N.,
Narita S.,
Himi T.
Publication year - 2004
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.2004.01964.x
Subject(s) - intercellular adhesion molecule 1 , intracellular , tumor necrosis factor alpha , cell adhesion molecule , adhesion , necrosis , microbiology and biotechnology , alpha (finance) , pathology , chemistry , immunology , biology , cancer research , medicine , construct validity , nursing , organic chemistry , patient satisfaction
Summary 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‐α (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‐α‐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‐α‐induced release sICAM‐1 occurred in a time‐ and concentration‐dependent manner. DEX 10 −6 m attenuated the TNF‐α‐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.