Clarithromycin inhibits rhinovirus-induced bacterial adhesions to nasal epithelial cells

The Laryngoscope (Oct 2009)

Jong Hwan Wang, MD, Si Hyeong Lee, MD, Hyun Ja Kwon, MSc, Yong Ju Jang, MD *

Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea

email: Yong Ju Jang (jangyj@amc.seoul.kr)

OBJECTIVES/HYPOTHESIS:: We investigated the inhibitory effects of clarithromycin (CM) on the rhinovirus (RV)-induced expression of fibronectin (Fn) and carcinoembryonic antigen-related cell adhesion molecules (CEACAMs), which act as major receptors for Staphylococcus aureus and Haemophilus influenzae, respectively. We further investigated the effects of CM on secondary S. aureus and H. influenzae adhesions to RV-infected primary human nasal epithelial cells (HNECs). 
METHODS:: Cells were pretreated with 10 muM CM 24 hours before RV-16 infection and for 48 hours thereafter. The expression levels of Fn and CEACAMs were assayed by reverse transcriptase-polymerase chain reaction and Western blotting. Bacterial adhesion to cells was assessed by confocal microscopy and the fluorescence intensity of adherent bacteria was analyzed using Image-Pro Plus 5.1 (Media Cybernetics, Bethesda, MD). 


RESULTS:: Clarithromycin significantly inhibited the RV-induced gene and protein expression of Fn and CEACAMs in HNECs. Compared with RV-infected cells, CM treatment significantly reduced the adhesion levels of S. aureus and H. influenzae in RV-infected HNECs to the levels seen in noninfected control cells. 


CONCLUSIONS:: These findings indicate that CM has the potential to prevent secondary bacterial infections in RV-infected HNECs by inhibiting the expression of Fn and CEACAM, thereby interfering with bacterial adhesion. 
Laryngoscope, 2009.