| Project/Area Number |
24591131
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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 |
Respiratory organ internal medicine
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| Research Institution | Kobe University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KOBAYASHI Kazuyuki 神戸大学, 大学院医学研究科, 講師 (50403275)
OKADA Taro 神戸大学, 大学院医学研究科, 准教授 (80304088)
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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 |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | スフィンゴシン1リン酸 / スフィンゴシン1リン酸受容体 / 喘息 / JTE013 / TSLP / IL-25 / IL-33 / 気管支喘息 / 樹状細胞 / 卵白アルブミン / マウス / 国際情報交換 / 気道炎症 / 気道リモデリング / 治療 |
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| Outline of Final Research Achievements |
Sphingosine kinase phosphorylates sphingosine to generate sphingosine 1 phosphate (S1P). S1P stimulates the five S1P receptors (S1PR), but S1PRs’ roles in the respiratory system and the therapeutic effect of S1PR antagonist in experimental asthma mouse model are not well understood. Bronchial epithelial cells in mouse lung expressed S1PR1 to 3. S1P induced proinflammatory cytokine production by the bronchial epithelial cells. In experimental asthma model, JTE013 exhibited substantially attenuated eosinophilic inflammation. In conclusion, JTE013 attenuated eosinophilic inflammation via regulating proinflammatory cytokines from bronchial epithelial cells. Our results suggest that JTE013 might be a possible candidate for the bronchial asthma treatment.
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