| Project/Area Number |
18K15913
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 53030:Respiratory medicine-related
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2020: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 気管支喘息 / IL-13 / LC3 / air-liquid interface / Quantitative PCR / Western blotting / BEAS-2B / 走査電子顕微鏡 / 培養条件 / 喘息 |
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| Outline of Final Research Achievements |
We examined each matter by using the purchased cells (BEAS-2B) in an air-liquid interface (ALI), which is a culture method that imitates the human airway environment. First, we compared the control group with the IL-13-added group. The results of the scanning electron microscope showed some changes in the IL-13-added group, but no significant changes were observed in the other studies. Therefore, we conducted a study using cells obtained from asthmatic or non-asthmatic patients, but no significant difference has been observed here either. So, we are reexamining the culture conditions and also examining using different cell lines in parallel.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、まだ、ヒトの気道環境を模した気道上皮培養方法（ALI）を用いて、IL-13付加によって気管支喘息と同様の気道上皮の変化があることを確認するところまでにとどまっている。しかしながら、現在検討している条件が整うことで先の検討へ進むことができれば、Autophagyには細胞からの分泌を促進する機構が存在することも指摘されており、Autophagy関連タンパクであるLC3を制御することで気道上皮細胞からのムチン産生が抑制されることが予想される。LC3を制御することでムチン産生が抑制されれば、重症喘息を含む様々な難治性の呼吸器疾患の増悪の抑制または病態の改善に大いに役立つと考えられる。
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