Experimental rhinovirus 16 infection increases intercellular adhesion molecule-1 expression in bronchial epithelium of asthmatics regardless of inhaled steroid treatment

Background Rhinovirus infections in airway epithelial cells in vitro have b een shown to upregulate intercellular adhesion molecule-1 (ICAM-1) expressi on. Epithelial ICAM-1, in its dual role as the major rhinovirus receptor an d as adhesion molecule for inflammatory cells may be involved in the pathog enesis 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 asth ma. In addition, the effect of 2 weeks pretreatment with inhaled budesonide (800 mu g b.d.) on RV16-associated changes in ICAM-1 expression was studie d. Methods The study had a parallel, placebo-controlled design in 25 steroid-n aive nonsmoking atopic asthmatic subjects. After 2 weeks budesonide (BUD) o r placebo (PLAC) pretreatment bronchoscopy was performed 2 days before (day -2) and 6 days after (day 6) RV16 inoculation (on days 0 and 1). Immunohis tochemical staining for ICAM-1 was performed on snap-frozen bronchial biops ies. ICAM-1 staining intensity on the basal epithelial cells was scored sem iquantitatively from 1 (weak) to 3 (intense). Similarly, epithelial intactn ess was noted (1 = basal cells only, 2 = basal and parabasal cells, 3 = int act epithelium). Results ICAM-1 scores were not significantly different between the groups a t day -2 (P greater than or equal to 0.08), Subsequent RV16 infection was a ssociated 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 t he groups before RV16 infection (P greater than or equal to 0.07), and no s ignificant changes were observed in either group (P greater than or equal t o 0.59). Moreover, ICAM-1 score did not correlate significantly with epithe lium score in either group, at any time-point (P greater than or equal to 0 .27). Conclusion We conclude that an RV16 common cold in atopic asthmatic subject s is associated with increased ICAM-1 expression in the bronchial epitheliu m, 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 agai nst the spreading of infection during rhinovirus-induced exacerbations in a sthma.