2016 Fiscal Year Final Research Report
Investigation for the mechanism of macrolide and development for combination therapy with macrolide
Project/Area Number |
26462578
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Otorhinolaryngology
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Research Institution | Mie University |
Principal Investigator |
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Keywords | MUC5AC / マクロライド / MKP-1 / p38 |
Outline of Final Research Achievements |
Low-dose, long-term macrolide therapy is effective in patients with chronic airway diseases such as diffuse panbronchitis, chronic bronchitis, and chronic sinusitis. However, the mechanism underlying this clinical efficacy remains unclear. It was recently reported that MKP-1 appears to mediate the effects of several anti-inflammatory drugs, including glucocorticoids, but the role of MKP-1 on mucin gene expression in the presence of macrolide remains unknown in human airways. Here, we show that MKP-1protein is induced by clarithromycin, and that clarithromycin suppresses TNF-α-induced MUC5AC mucin gene expression in a p38 MAPK-dependent manner in human airway epithelial cells, NCI-H292 cells. Our study thus provides new insights into the role of MKP-1 on the effect of macrolides, and may help in the development of new therapeutic strategies against mucin overproduction.
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Free Research Field |
耳鼻咽喉科
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