Effects of Clarithromycin on Cultured Human Nasal Epithelial Cells and Fibroblasts

Abstract Objective/Methods: Long‐term administration of clarithromycin has been reported to be effective in the treatment of chronic sinusitis. To investigate the mechanism underlying the anti‐inflammatory activity of clarithromycin, the authors evaluated the effect of clarithromycin on the gene expression of proinflammatory cytokine and the DNA‐binding activity of nuclear factor (NF)‐κB in cultured human nasal epithelial cells and fibroblasts. Cells were incubated with endotoxin purified from nontypeable Haemophilus influenzae or interleukin (IL)‐1β in the presence of clarithromycin. Results: Northern blot analysis revealed that clarithromycin suppressed IL‐1β gene expression in human nasal epithelial cells stimulated by H influenzae endotoxin (HIE). Intercellular adhesion molecule‐1 gene expression in nasal fibroblasts stimulated by IL‐1β was also suppressed by clarithromycin. Furthermore, electrophoretic mobility shift assay demonstrated that clarithromycin reduced DNA‐binding activity of NF‐κB in both human nasal epithelial cells and fibroblasts stimulated by HIE or IL‐1β, respectively. Conclusion: The present results suggest that clarithromycin may reduce gene expression of proinflammatory cytokines and adhesion molecules from nasal mucosa at the transcriptional factor level and exert an anti‐inflammatory effect on nasal mucosa in chronic sinusitis.