| Project/Area Number |
17K09662
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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 | Sapporo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
高橋 素子 札幌医科大学, 医学部, 教授 (00303941)
千葉 弘文 札幌医科大学, 医学部, 准教授 (40347175)
大塚 満雄 札幌医科大学, 医学部, 研究員 (10398323)
黒沼 幸治 札幌医科大学, 医学部, 講師 (40563250)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 肺サーファクタント / 肺傷害 / 間質性肺炎 / 内科 / 免疫学 |
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| Outline of Final Research Achievements |
Objective: To develop a new therapeutic method for idiopathic pulmonary fibrosis under the hypothesis that surfactant protein (SP) -A supplementation and HSP47 siRNA suppress lung inflammation and fibrosis. Method: BLM was intratracheally administered to SP-A (-/-) and wild-type mice to prepare a lung injury / fibrosis model, and siRNA HSP47 was intravenously administered. Results: Inflammation and fibrosis were enhanced in SP-A deficient mice compared to wild type. In addition, siRNA HSP47 reduced lung injury and suppressed BLM-induced airway inflammation. Conclusion: SP-A supplementation and siRNA HSP47 suppressed the formation of lung injury / fibrotic lesions, and it was shown that the combination of both could be one of the new treatments for pulmonary fibrosis.
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| Academic Significance and Societal Importance of the Research Achievements |
特発性肺線維症は予後が三年程度の難治性疾患であり、自然免疫の破綻と線維の過剰産生が悪化のメカニズムに関与している。肺線維症の動物モデルで検討した結果、自然免疫調整因子であるサーファクタント蛋白質(SP)-Aが欠損すると病変が悪化し、また、siRNA HSP47で線維生成を抑制することによって悪化が抑制された。したがって、両者の併用が肺線維症の新たな治療法のひとつになりうることが示された。
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