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2018 Fiscal Year Final Research Report

Development of novel treatment for severe obesity asthma

Research Project

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Project/Area Number 16K19448
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Respiratory organ internal medicine
Research InstitutionHamamatsu University School of Medicine

Principal Investigator

SUZUKI YUZO  浜松医科大学, 医学部, 助教 (00758435)

Project Period (FY) 2016-04-01 – 2019-03-31
Keywords肥満喘息 / 重症喘息 / オートファジー / アレルギー
Outline of Final Research Achievements

Close associations between obesity and severe asthma have epidemiologically reported. However, little is known about underlying mechanism. We investigated the pathogenesis of autophagy in development of severe obesity induced asthma. We found that high-fat diet induced autophagy deficient obesity mice (Atg5-/- obesity mice) developed severe asthma in terms of elevated eosinophilic inflammation together with increased airway hyperreactivity (AHR). Furthermore, increased eosinophil inflammation and AHR in Atg5-/- obesity mice was TSLP dependent. Our results showed autophagy is involved in the pathogenesis of obesity induced severe eosinophilic asthma and can be a novel therapy target for these patients.

Free Research Field

呼吸器内科

Academic Significance and Societal Importance of the Research Achievements

肥満喘息の難治化の要因を、生体の恒常性維持に必須であるオートファジーに注目して解析した。本研究ではオートファジー低下によってもたらされる気道上皮関連サイトカイン:TSLP上昇が病因に関与すると考えられた。成人肥満の増加のみならず小児肥満の増加も報告され、肥満による喘息コントロールの難治化、重症化がは今後の喘息診療の大きな課題になると考えられる。そのため、本研究で得られた知見は非常に重要である。さらに、オートファジー制御は重症肥満喘息の新規治療標的の候補になると考えられた。

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Published: 2020-03-30  

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