Levocetirizine inhibits rhinovirus-induced bacterial adhesion to nasal epithelial cells through down-regulation of cell adhesion molecules

Background: The first critical step for bacterial infection is attachment of bacteria to the cell adhesion molecules of epithelial cells. The rhinovirus (RV)-induced increased expression of cell adhesion molecules including fibronectin (Fn) and carcinoembryonic antigen-related cell adhesion molecules (CEACAMs) is closely related to the activation of nuclear factor-kappa B (NF-kappa B). Recent studies have demonstrated that Levocetirizine (LCT) has anti-inflammatory properties that are mediated by inhibitory effects on NF-kappa B in addition to classic antihistaminic effects. Objective: To investigate the inhibitory effects of LCT on the RV-induced expression of Fn and CEACAMs in human nasal epithelial cells (HNECs) and identified the effects of LCT on secondaryStaphylococcus aureus and Haemophilus influenzae adhesion to RV-infected HNECs. Methods: Primary HNECs obtained from inferior turbinate mucosa were pretreated with 50 nM LCT 24 hours before RV-16 infection and for 48 hours thereafter. The expression levels of Fn and CEACAMs were assayed by real-time polymerase chain reaction (PCR) and Western blotting. Bacterial adhesion to cells was assessed by confocal microscopy. Results: Fibronectin and CEACAM messenger RNA (mRNA) and protein levels in HNECs were significantly increased by RV-16 infection. Levocetirizine significantly reduced these increases in mRNA levels and protein expression of Fn and CEACAMs. Confocal microscopy showed that treatment with LCT significantly reduced the adhesion levels of S aureus and H influenza in RV-infected HNECs compared with RV-infected, untreated HNECs. Conclusion: These findings suggest that LCT inhibits the expression of Fn and CEACAMs and has the potential to prevent secondary bacterial infections in RV-infected HNECs by interfering with bacterial adhesion. (C) 2012 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.