| 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 |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Mie University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | MUC5AC / マクロライド / MKP-1 / ｐ３８ / クラリスロマイシン / p38 / 作用機序 |
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| 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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