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The role of TRP channel in the pathogenesis of antigen-nonspecific asthma exacerbation

Research Project

Project/Area Number 16K09583
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Respiratory organ internal medicine
Research InstitutionKagoshima University

Principal Investigator

Machida Kentaro  鹿児島大学, 医歯学域附属病院, 助教 (90597569)

Co-Investigator(Kenkyū-buntansha) 井上 博雅  鹿児島大学, 医歯学域医学系, 教授 (30264039)
Research Collaborator Takagi koichi  
Mathuhyama Takahiro  
Project Period (FY) 2016-04-01 – 2019-03-31
Project Status Completed (Fiscal Year 2018)
Budget Amount *help
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
KeywordsTRPチャンネル / 気管支喘息 / 気道炎症 / 温度変化 / 免疫制御機構 / 神経伝達物質 / 自然免疫 / 獲得免疫 / TPRチャンネル / 喘息 / アレルギー性気道炎症 / TRP / ぜんそく
Outline of Final Research Achievements

Asthmatic patients sometimes experience exacerbation by changes in temperature, but the precise mechanism is unknown. In this study, we investigated the involvement of TRP-X channel in the pathogenesis of temperature evoked asthma exacerbation using genetically modified mice of TRP-X channel involved in various biological functions as sensors that sense chemical and physical stimuli. Mice were exposed to cold temperature stimuli with papain administration intra-nasally, wild type mice showed exacerbation of eosinophilic airway inflammation compared to papain administration alone. On the other hand, in TRP-X channel genetically modified mice, cold temperature induced exacerbation of eosinophilic airway inflammation was suppressed. This study revealed that TRP-X channel is involved in the pathogenesis of cold temperature induced exacerbation of eosinophic airway inflammation in asthma.

Academic Significance and Societal Importance of the Research Achievements

本研究により、今までに十分には明らかにされていない温度変化による喘息増悪のメカニズムに、TRPチャンネルが関与しているとが明らかとなった。今後更に詳細な分子メカニズムを明らかにする事によって、TRPチャンネルやそのシグナル経路を標的とした新たな創薬に繋がることが期待される。

Report

(4 results)
  • 2018 Annual Research Report   Final Research Report ( PDF )
  • 2017 Research-status Report
  • 2016 Research-status Report
  • Research Products

    (4 results)

All 2019 2018 2017 2016

All Presentation (4 results) (of which Int'l Joint Research: 3 results,  Invited: 1 results)

  • [Presentation] TRPA1-deficient mice were suppressed airway inflammation in a papain induced model2019

    • Author(s)
      Takahiro Mathuhyama, Kentaro Machida, Kota Sakaue, Koichi Takagi, Hiromasa Inoue
    • Organizer
      American Thoracic Society 2019
    • Related Report
      2018 Annual Research Report
    • Int'l Joint Research
  • [Presentation] Type 2 innate lymphoid cells expressing death receptor 3 are increased in airway of mild atopic asthmatic subject following allergen inhalation challenges2018

    • Author(s)
      Kentaro Machida
    • Organizer
      2018 AAAAI/WAO Joint Congress
    • Related Report
      2017 Research-status Report
    • Int'l Joint Research
  • [Presentation] Type 2 Innate Lymphoid Cells Up-Regulate DR3 Expression Upon Stimulation with IL-2 and IL-332017

    • Author(s)
      Kentaro Machida
    • Organizer
      American Thoracic Society 2017
    • Related Report
      2017 Research-status Report
    • Int'l Joint Research
  • [Presentation] 喘息の病態と分子標的薬の可能性…重症喘息に対する分子標的薬の進歩2016

    • Author(s)
      井上博雅
    • Organizer
      第65回日本アレルギー学会学術大会
    • Place of Presentation
      東京国際フォーラム(東京都・千代田区)
    • Year and Date
      2016-06-17
    • Related Report
      2016 Research-status Report
    • Invited

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Published: 2016-04-21   Modified: 2020-03-30  

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