| Project/Area Number |
24592580
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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 | Juntendo University |
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Principal Investigator |
MIWA Masato 順天堂大学, 医学部, 准教授 (80247650)
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| Co-Investigator(Kenkyū-buntansha) |
KAMIYA Kazusaku 順天堂大学, 医学部, 准教授 (10374159)
IKEDA Katsuhisa 順天堂大学, 医学部, 教授 (70159614)
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| Co-Investigator(Renkei-kenkyūsha) |
TAKAI Toshiro 順天堂大学, 医学部, 准教授 (70338375)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | バリア機能 / フィラグリン / アレルギー性鼻炎 / 花粉症 / 鼻粘膜上皮 / ドライノーズ / 花粉症の初期治療 / アレルギーの先制医療 / 鼻粘膜上皮バリア機能 / TSLP / LPS / poly I:C / PolyI: C / スギ花粉症 / アレルギーマーチ / 早期介入 / 上皮水分蒸散量 / 上皮間電位差 |
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| Outline of Final Research Achievements |
Filaggrin (FLG) has been known as a natural moisturizing factor and barrier related protein.
We have demonstrated the expression of FLG through real time RT-PCR in human nasal mucosa excised from inferior turbinate by a noninvasive method using cotton swab. Preseasonal treatment of Japanese cedar pollinosis with antihistamine increased FLG expression in human nasal mucosa compared with postseasonal treatment.Additionally, we are investigating the alteration of FLG expression in primary cultured human nasal epithelial cells through various stimulations. After stimulation of lipopolysaccharide (LPS), poly I: C, FLG expression was diminished. On the other hand, TNFα increases FLG expression in primary cultured cells.Taken together recent reports and our original results, FLG might be a key molecule connecting innate immunity with acquired immunity in the upper airway. Further study would be expected to fix the epithelial barrier to treat and prevent AR as a barrier disorder.
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