| Project/Area Number |
15H04828
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Chiba University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
玉地 智宏 千葉大学, 大学院医学研究院, 助教 (20456015)
須藤 明 千葉大学, 大学院医学研究院, 准教授 (50447306)
廣瀬 晃一 千葉大学, 大学院医学研究院, 准教授 (90400887)
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| Research Collaborator |
HIROSE Koichi
ITO Takashi
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2017: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2015: ¥6,630,000 (Direct Cost: ¥5,100,000、Indirect Cost: ¥1,530,000)
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| Keywords | 喘息 / IL-22 / Reg3g / 気道上皮 / Reg3gamma / アレルギー・ぜんそく / 糖鎖修飾 / 気道上皮細胞 / レクチン受容体 / IkBNS |
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| Outline of Final Research Achievements |
We analyzed the role of IL-22 in regulating allergic airway inflammation. We show that allergic airway inflammation and Th2 and Th17 cytokine production upon intratracheal administration of house dust mite extract (HDM) were exacerbated in IL-22-deficient mice. We also found that IL-22 induces Reg3g production from lung epithelial cells through STAT3 activation and that neutralization of Reg3g significantly exacerbates HDM-induced eosinophilic airway inflammation and Th2 cytokine induction. Moreover, EXTL3, a functional Reg3g binding protein, is expressed in lung epithelial cells, and intratracheal administration of recombinant Reg3g suppresses HDM-induced TSLP and IL-33 expression and accumulation of type 2 innate lymphoid cells in the lung. Taken together, these results suggest that IL-22 induces Reg3g production from lung epithelial cells and inhibits the development of HDM-induced allergic airway inflammation possibly by inhibiting cytokine production from lung epithelial cells.
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