| Project/Area Number |
16K09569
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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 | Tohoku University |
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Principal Investigator |
KOARAI AKIRA 東北大学, 大学病院, 助教 (80458059)
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| Research Collaborator |
AIZAWA Hiroyuki
HIRANO Taizou
SHISHIKURA Yutaka
YANAGISAWA Satoru
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | IL-33 / 慢性閉塞性肺疾患 / 酸化ストレス / 自然リンパ球 / 閉塞性肺疾患 / アラーミン / 気道上皮 |
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| Outline of Final Research Achievements |
In chronic obstructive pulmonary disease (COPD), the morbidity and mortality have been increasing. Exacerbations of COPD lead to an increase in mortality and healthcare costs, therefore, the prevention and better understanding of the mechanisms is still needed.
To elucidate the involvement of innate lymphoid cells in the pathogenesis of COPD and the regulatory mechanism, we performed the current study. However, in our current protocol, it was difficult to identify the innate lymphoid cells because of the limitation of the cell number from the lung resection sample. On the other hand, IL-33 has been shown to act as a potent activator of innate lymphoid cells, therefore, we also evaluated the regulation mechanism of IL-33 in COPD. In the current study, we first demonstrated that oxidative stress may participate in the regulation of IL-33 expression in airway epithelial cells in COPD. Modulation of this pathway could become a therapeutic target for viral-induced exacerbations of COPD.
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| Academic Significance and Societal Importance of the Research Achievements |
慢性閉塞性肺疾患（COPD）は有病率及び死亡率は年々増加しており、COPDの管理において急性増悪の制御はその病態進行のみならず入院費増大など社会的負荷の観点からも必要不可欠である。近年、COPD増悪病態への自然リンパ球の関与が注目されており、本研究では自然リンパ球の活性化に関わるIL-33の気道上皮における発現が酸化ストレスにより調節されることをCOPDにおいて初めて報告し、この機序を修飾することがウイルス感染を契機としたCOPD増悪に対する新たな治療戦略の１つとなる可能性を示した。
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