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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Anti-Bacterial Agents, Bacterial Adhesion, Cell Adhesion Molecules, Cells, Cultured, Clarithromycin, Fibronectins, Haemophilus influenzae, Humans, Nasal Mucosa, Polymerase Chain Reaction, Rhinovirus, Staphylococcus aureus.
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Does clarithromycin inhibit rhinovirus-induced bacterial adhesions to nasal epithelial cells? Context: 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). Cells were pretreated with 10 microM 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). 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.
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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. Final Decision: yes