| Project/Area Number |
26670746
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
Himi Tetsuo 札幌医科大学, 医学部, 教授 (90181114)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | ＲＳウイルス / インターフェロン / ＩＲＦ３ / 鼻粘膜 / 上皮細胞 / クラリスロマイシン / サイトカイン / .上気道感染 / Ⅲ型インターフェロン / 抗ウイルス作用 / ストレス顆粒 / ムンプスウイルス / ウイルス感染 / microRNA / ウイルス持続感染 |
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| Outline of Final Research Achievements |
Human respiratory syncytial virus (RSV) infects to airway epithelium cells, and causes frequently bronchiolitis and pneumonia in infants. Clarithromycin (CAM), which is a one of the macrolide antimicrobial agents, is also known as an immunomodulator, and has been used for otitis media with effusion and chronic sinusitis.CAM suppresses the production of pro-inflammatory cytokines and IFNs induced by virus-related stimuli, such as RSV and poly I:C. CAM exerts these effects by inhibiting the dimerization and subsequent nuclear translocation of IRF3 in airway epithelial cells.
CAM also dramatically suppressed RSV-induced promoter activity of the PRDIII-I, which is an IRF3 biding element. RSV-induced phosphorylation of IRF-3 did not alter in the presence of CAM. CAM inhibits IRF3 dimerization and its subsequent nuclear translocation from cytosol upon stimulation with poly I:C or RSV.
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