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Experimental rhinovirus 16 infection increases intercellular adhesion molecule‐1 expression in bronchial epithelium of asthmatics regardless of inhaled steroid treatment
Author(s) -
Van Krieken J. Han J. M.
Publication year - 2000
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 - 10.1046/j.1365-2222.2000.00854.x
Subject(s) - rhinovirus , budesonide , icam 1 , intercellular adhesion molecule 1 , respiratory epithelium , basal (medicine) , epithelium , immunology , respiratory tract , medicine , fluticasone , placebo , asthma , inflammation , cell adhesion molecule , pathology , respiratory system , alternative medicine , insulin
Background Rhinovirus infections in airway epithelial cells in vitro have been shown to upregulate intercellular adhesion molecule‐1 (ICAM‐1) expression. Epithelial ICAM‐1, in its dual role as the major rhinovirus receptor and as adhesion molecule for inflammatory cells may be involved in the pathogenesis of rhinovirus‐induced exacerbations of asthma. Objective We aimed to investigate the effect of experimental rhinovirus 16 (RV16) infection on ICAM‐1 expression in bronchial mucosal biopsies in asthma. In addition, the effect of 2 weeks pretreatment with inhaled budesonide (800 μg b.d.) on RV16‐associated changes in ICAM‐1 expression was studied. Methods The study had a parallel, placebo‐controlled design in 25 steroid‐naive nonsmoking atopic asthmatic subjects. After 2 weeks budesonide (BUD) or placebo (PLAC) pretreatment bronchoscopy was performed 2 days before (day −2) and 6 days after (day 6) RV16 inoculation (on days 0 and 1). Immunohistochemical staining for ICAM‐1 was performed on snap‐frozen bronchial biopsies. ICAM‐1 staining intensity on the basal epithelial cells was scored semiquantitatively from 1 (weak) to 3 (intense). Similarly, epithelial intactness was noted (1 = basal cells only, 2 = basal and parabasal cells, 3 = intact epithelium). Results ICAM‐1 scores were not significantly different between the groups at day −2 ( P ≥ 0.08). Subsequent RV16 infection was associated with a trend towards an increase in ICAM‐1 expression in the BUD‐group ( P = 0.07), whereas the increase was significant in the PLAC‐group ( P = 0.03). However, the increase was not significantly different between the groups ( P = 0.74). Epithelial intactness score was not different between the groups before RV16 infection ( P ≥ 0.07), and no significant changes were observed in either group ( P ≥ 0.59). Moreover, ICAM‐1 score did not correlate significantly with epithelium score in either group, at any time‐point ( P ≥ 0.27). Conclusion We conclude that an RV16 common cold in atopic asthmatic subjects is associated with increased ICAM‐1 expression in the bronchial epithelium, which is not related to epithelial intactness. Glucocorticoid treatment does not appear to prevent the RV16‐associated increased ICAM‐1 expression. This suggests that other treatment modalities are required to protect against the spreading of infection during rhinovirus‐induced exacerbations in asthma.