Expression of intercellular adhesion molecule-1 (ICAM-1) in nasal epithelial cells of atopic subjects: a mechanism for increased rhinovirus infection?

Since clinical experimental studies indicate that upper respiratory tract v iral infections may exacerbate acute asthma symptoms in atopic/asthmatic in dividuals, we have investigated the expression and modulation of ICAM-1 on human nasal epithelial cells (HNEC) from normal and atopic subjects. ICAM-1 is the attachment molecule for the majority of serotypes of human rhinovir us (HRV), including HRV-14, and is also critical for the migration and acti vation of immune effector cells. Basal ICAM-1 expression was significantly higher in HNEC obtained by brushings from atopic compared with non-atopic s ubjects (P = 0.031), and was also significantly increased on atopic HNEC ha rvested in season compared with out of season (P < 0.05). Atopic HNEC showe d further up-regulation in ICAM-1 expression when cultured with clinically relevant allergen (P = 0.032). ICAM-1 levels on normal HNEC were also incre ased by infection with HRV-14 (P < 0.05). Basal expression of ICAM-1 on ato pic nasal polyp epithelial cells (EC) was significantly higher than on both normal and atopic nasal HNEC. This elevated nasal polyp ICAM-1 level was n ot increased further by allergen, although HRV infection resulted in a smal l significant increase. Recovered viral titres from HRV-infected nasal poly p EC were 1.5-fold higher than from infected normal nasal HNEC. The data ar e consistent with the hypothesis that allergen, by enhancing expression of the HRV attachment target on host cells, facilitates viral infection in ato pic subjects; simultaneously HRV-induced increases in ICAM-1 levels would f avour migration and activation of immune effector cells to the airway, resu lting in enhanced atopic inflammation.