Development of a therapeutic method for asthma exacerbation with cross-talk of immune- and peripheral nervous-system
| Project/Area Number |
17K16064
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Respiratory organ internal medicine
|
|---|
| Research Institution | Kyoto University (2020-2022)
Tokyo Women's Medical University (2017-2019) |
|---|
Principal Investigator |
ASHINO Shigeru 京都大学, オープンイノベーション機構, 特定講師 (10507221)
|
|---|
| Project Period (FY) |
2017-04-01 – 2023-03-31
|
| Project Status |
Completed (Fiscal Year 2022)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| Keywords | 気管支喘息 / ウイルス感染 / 難治性気管支喘息 / アレルギー・ぜんそく / ウィルス感染 / 重症気管支喘息 / ウィルス / 免疫学 |
|---|
| Outline of Final Research Achievements |
In the present study, an asthma exacerbation model mouse using a viral component poly I:C, which mimics virus infection, was successfully established. It was revealed that the airway hyperresponsiveness was higher in the poly I:C-induced asthma exacerbation model compared to regular asthma model. In addition, neutrophilic airway inflammation with pulmonary Th1/Th17 cytokines were upregulated in the asthma exacerbation model.
Moreover, a neuro-transmitter peptide receptor expressing dendritic cells and macrophases were involved in the asthma exacerbation phenotype. We found that an antagonist against the neuro peptide was capable of controlling the exacerbated pathogenesis.
These results suggest that the cross-talk of immune cells and the neuro peptide could be therapeutic target to negatively regulate the exacerbation.
|
| Academic Significance and Societal Importance of the Research Achievements |
本研究では、ウイルス感染状態にある喘息増悪メカニズムの一端をマウスを使った実験で示し、その制御法開発の研究基盤の構築を進めた。その結果、ヒトでも確認される増悪メディエーターの肺内での上昇が認められ、その病態において神経ペプチドの一種の受容体を発現する免疫細胞 (樹状細胞やマクロファージ) が標的になる可能性が示唆された。現在の重症喘息に適応されているサイトカイン中和抗体製剤が無効である場合に、この新規知見を応用することが可能かどうか検討を続けている。
|
Report
(7 results)
Research Products
(6 results)
