| Project/Area Number |
16K19608
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Collagenous pathology/Allergology
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| Research Institution | Tohoku Medical and Pharmaceutical University |
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Principal Investigator |
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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 |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 気道上皮細胞 / 喘息 / 性差医学 / 樹状細胞 / 気管支喘息 / 女性 / 増悪 / 性差医療 / アレルギー内科学 / アレルギー・ぜんそく / 免疫学 |
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| Outline of Final Research Achievements |
To address the pathways mediating sex disparities in the severity of adult asthma, in the present study we examined the sex-related influence of airway epithelial cells on lung DC activation using an ovalbumin (OVA)-induced asthma mouse model. Airway epithelial cells (CD31- CD45- Ep-CAM+ cells), regulators of airway inflammation, from asthmatic female mice expressed higher levels of Il-33 and Ccl2 at 1 and 4 h after OVA inhalation, respectively, compared with those in male mice. The enhanced IL-33 production from airway epithelial cells in female mice may be associated with enhanced CD86 expression on DCs. These results suggest that airway epithelial cells may contribute to female-predominant Th2 cytokine production through activation of DCs in asthma.
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| Academic Significance and Societal Importance of the Research Achievements |
喘息の増悪による救急外来受診後の再発率や入院治療にかかる医療費は男性患者より女性患者において高く、病態重症化および医療経済的視点から女性における喘息重化の問題の解決は社会的要請が高い。本研究は、喘息における免疫学的メカニズムの性差に着目し、炎症の起点である気道上皮細胞におけるサイトカインとケモカイン産生の増加が女性における喘息病態の増悪に関与している可能性を明らかにした。本研究の成果は、女性における喘息の増悪において、気道上皮細胞が主要な治療標的になり得る可能性を示唆するものである。
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