Roxithromycin Suppresses MUC5B/8 Mucin Genes and Mucin Production in Airway Epithelial Cells.
- Author:
Hyun Jae WOO
1
;
Myung Ki MIN
;
Chang Hoon BAE
;
Si Youn SONG
;
Yong Dae KIM
Author Information
1. Department of Otorhinolaryngology-Head and Neck Surgery, College of Medicine, Yeungnam University, Daegu, Korea. ydkim@med.yu.ac.kr
- Publication Type:Original Article
- Keywords:
Airway;
Roxithromycin;
Mucin;
MUC5B;
MUC8
- MeSH:
Anti-Bacterial Agents;
Epithelial Cells;
Gene Expression;
Humans;
Inflammation;
Macrolides;
Mucins;
Mucus;
Nasal Polyps;
Roxithromycin
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2008;51(7):617-622
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: Macrolide antibiotics are known to inhibit mucus hypersecretion in patients with chronic airway diseases, but its action mechanism is unclear. Several reports demonstrated that macrolides significantly inhibited gene expression of MUC2, MUC4 and MUC5AC in the airway epithelial cells, but little is known about its inhibitory effect for the other important airway mucins. In upper airway tracts, MUC5B and MUC8 are other important secreted mucin genes. Therefore, this study was aimed to investigate the effects of roxithromycin on the IL-1beta-induced gene expression and mucin production of MUC5B and MUC8 in NCI-H292 cells and cultured human nasal polyp epithelial cells. SUBJECTS AND METHOD: The effects of roxithromycin on the IL-1beta-induced MUC5B and MUC8 expression were analyzed by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. RESULTS: Roxithromycin attenuated the IL-1beta-induced MUC5B and MUC8 gene expression and mucin production with a dose-dependent pattern in NCI-H292 epithelial cells and cultured human nasal polyp epithelial cells. CONCLUSION: Roxithromycin exerts direct inhibitory effects on the gene expression of MUC5B and MUC8 in airway epithelial cells. These novel findings may explain the clinical efficacy of 14-membered macrolides in the treatment of chronic airway inflammations.
