2022 Fiscal Year Final Research Report
The role of glycosylation in airway epithelium in the pathogenesis of bronchial asthma
Project/Area Number |
20K08569
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 53030:Respiratory medicine-related
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Research Institution | Kagoshima University |
Principal Investigator |
Momi Hiroaki 鹿児島大学, 医歯学総合研究科, 客員研究員 (90794157)
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Co-Investigator(Kenkyū-buntansha) |
井上 博雅 鹿児島大学, 医歯学域医学系, 教授 (30264039)
高木 弘一 鹿児島大学, 医歯学総合研究科, 特任助教 (40707866)
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | 気管支喘息 / 自然リンパ球 / 糖鎖修飾 / 好中球性炎症 |
Outline of Final Research Achievements |
We investigated the mechanism of refractory bronchial asthma by focusing glycan modification changes in airway epithelial cells by type 3 innate lymphocytes (ILC3). Regarding glycan modification of airway epithelial cells, we analyzed exosomes derived from airway epithelial cells, and showed that the glycan structure expressed on the exosome matches the glycan structure of the derived cell. In addition, since ILC3 in asthma is involved in neutrophilic inflammation, we analyzed the pathophysiology of asthma by creating asthma model mice that cause neutrophilic inflammation and studied the involvement of ILC3 in the severity of asthma. This study suggests that glycosylation in airway epithelial cells is involved in the pathogenesis of asthma.
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Free Research Field |
喘息・COPD
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Academic Significance and Societal Importance of the Research Achievements |
喘息難治化の病態の一つに、好中球性炎症が関わっていることが示されている。今回の研究において、好中球性炎症を伴う喘息について、新たにILC3や気道上皮細胞における糖鎖修飾などの関与が示唆されている。更に研究を進めることでこの機序が明らかになれば、難治性喘息における新規治療標的の開発につながる可能性がある。
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