| Project/Area Number |
26290031
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Laboratory animal science
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| Research Institution | Kyoto University |
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Principal Investigator |
Kuramoto Takashi 京都大学, 医学(系)研究科(研究院), 准教授 (20311409)
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| Co-Investigator(Kenkyū-buntansha) |
椛島 健治 京都大学, 医学(系)研究科(研究院), 教授 (00362484)
吉見 一人 国立遺伝学研究所, 大学共同利用機関等の部局等, 助教 (50709813)
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| Co-Investigator(Renkei-kenkyūsha) |
HIAI Hiroshi 京都大学, 名誉教授 (10073131)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥16,900,000 (Direct Cost: ¥13,000,000、Indirect Cost: ¥3,900,000)
Fiscal Year 2016: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2015: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2014: ¥7,540,000 (Direct Cost: ¥5,800,000、Indirect Cost: ¥1,740,000)
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| Keywords | アトピー性皮膚炎 / ラット / 疾患モデル / IgE / 引掻き行動 / 好酸球 / マスト細胞 / ステロイド / ハプテン / アレルギー・ぜんそく / 免疫学 / 薬理学 / 応用動物 / タクロリムス / 引っかき行動 |
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| Outline of Final Research Achievements |
Rats showing spontaneous atopic dermatitis (AD)-like skin lesions were observed in the Kyoto fancy rat stock 4 (KFRS4) rats. To establish the KFRS4 rat as a model of AD, clinical symptom, scratching behavior, and transepidermal water loss (TEWL) were examined. Dermatitis initially appeared around 4 months of age and rapidly worsened from 6 to 8 months of age. The skin lesions accompanied scratching behavior and were predominantly observed in females. The increased TEWL indicated skin barrier dysfunction. Extensive infiltration of eosinophils, mast cells and lymphocytes was observed in the skin lesions. The plasma IgE level increased in accord with increasing severity of dermatitis. The betamethasone improved the symptoms of dermatitis. These findings demonstrated that dermatitis in the KFRS4 rats closely resembled that seen in human AD, which suggested that female KFRS4 rats have the potential to serve as an animal model of human AD.
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