Analysis of anti-viral innate immunity and therapeutic strategies for upper respiratory disease.

2017 Fiscal Year Final Research Report

• Project/Area Number: 26293370
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Otorhinolaryngology
• Research Institution: Sapporo Medical University
• Principal Investigator: Himi Tetsuo 札幌医科大学, 医学部, 教授 (90181114)
• Co-Investigator(Kenkyū-buntansha): 横田 伸一 札幌医科大学, 医学部, 教授 (10325863) ; 高野 賢一 札幌医科大学, 医学部, 准教授 (70404689) ; 小笠原 徳子 札幌医科大学, 医学部, 助教 (00438061)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: 上気道感染 / ウイルス / RSウイルス / インターフェロン / IRF3 / 気道上皮細胞

Outline of Final Research Achievements

We examined the effect of CAM on production of cytokines, CAM significantly suppressed RSV-induced production of IFN-λ1, λ2 and λ3. CAM dramatically suppressed RSV-induced promoter activity, 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.
In conclusion, 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. NIP-SNAP and MuV-induced SGs partly suppressed viral-induced type Ⅲ IFN production and suppressed the production of pro-inflammatory cytokines.

Free Research Field

耳鼻咽喉科学