| Project/Area Number |
21591375
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | The Institute of Physical and Chemical Research |
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Principal Investigator |
YOSHIDA Hisahiro 独立行政法人理化学研究所, アレルギー免疫遺伝研究チーム, チームリーダー (20281090)
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| Co-Investigator(Renkei-kenkyūsha) |
安田 琢和 独立行政法人理化学研究所, アレルギー免疫遺伝研究チーム, 研究員 (00373374)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | アトピー性皮膚炎 / キチナーゼ様タンパク質 / 表皮バリア破壊 / 尋常性魚鱗癬 / Filaggrin / Tight junction / 衛生環境 / 信号伝達 / キチナーゼ様物質 / 皮膚免疫 / Th2誘導 / Chi3l1トランスジェニックマウス / Chi3l1KOマウス / Chitinase3like1 / 無菌飼育環境 / 皮膚常在細菌 / 黄色ブドウ球菌 / Th2からTh1への推移 / 自然免疫系 / Staphylococcus Aureus / 無菌状態下でのマウス / Spadeマウス / keratinocyte / 常在細菌 |
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| Research Abstract |
We have found the over expression of Chi3l1 in epidermis of the newly identified atopic dermatitis model mouse before the onset of disease. Overexpression of Chi3l1 transgene in epidermis resulted in skin barrier permeability destruction and ichthyosis vulgaris like appearance, In addition, in conventional condition, the AD model mouse showed similar appearance and tight junction protein expression was down-regulated. These findings indicated Chi3l1 protein play a role in skin barrier formation.
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