Investigation of the anti-viral mechanism by interference between lambda interferon subtypes

2015 Fiscal Year Final Research Report

• Project/Area Number: 26670746
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Otorhinolaryngology
• Research Institution: Sapporo Medical University
• Principal Investigator: Himi Tetsuo 札幌医科大学, 医学部, 教授 (90181114)
• Project Period (FY): 2014-04-01 – 2016-03-31
• 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

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.

Free Research Field

耳鼻咽喉科学