Project/Area Number |
20790697
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
膠原病・アレルギー・感染症内科学
|
Research Institution | University of Tsukuba |
Principal Investigator |
KAWAGUCHI Mio 筑波大学, 大学院・人間総合科学研究科, 講師 (50365748)
|
Co-Investigator(Renkei-kenkyūsha) |
HIZAWA Nobuyuki 筑波大学, 大学院・人間総合科学研究科, 教授 (00301896)
KOKUBU Fumio 昭和大学, 藤が丘病院呼吸器内科, 准教授 (21390254)
MATSUKURA Satoshi 昭和大学, 呼吸器アレルギー内科, 講師 (10384231)
|
Project Period (FY) |
2008 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2011: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2010: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2009: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2008: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
|
Keywords | 気管支喘息 / IL-17F / 気道リモデリング |
Research Abstract |
We discovered IL-17F gene in 2001, and have reported its function in asthma. However, the role of IL-17F in asthma has not been fully elucidated. Although inhaled corticosteroids are the most potent medicines for long-term control of asthma, anti-asthma medicines including inhaled corticosteroids are generally not so effective for severe asthma. To this end, treating sever asthma is future serious problem in the world. Airway remodeling is deeply involved in the pathogenesis of severe asthma. Airway remodeling is caused by, at least partially, a complicated network of cytokines, including IL-11 and insulin-like growth factor-I (IGF-I). To clarify the pathogenesis of airway remodeling in asthma, we investigated the induction of IL-11 and IGF-I by IL-17F in bronchial epithelial cells. IL-17F is able to induce IL-11 and IGF-I via Raf1-MEK1/2-ERK1/2-MSK1/p90RSK-CREB signaling pathway in bronchial epithelial cells. Hence, the IL-17F/IGF-I axis may be involved in airway inflammation and remodeling. Therefore, IL-17F and its signaling pathway may be a valuable therapeutic target for sever asthma.
|