2022 Fiscal Year Final Research Report
The role of cochlear resident macrophages in age-related hearing loss
Project/Area Number |
19K09908
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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 56050:Otorhinolaryngology-related
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Research Institution | Kyoto University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
西村 幸司 滋賀県立総合病院(研究所), その他部局等, 嘱託研究員 (20405765)
山本 典生 京都大学, 医学研究科, 准教授 (70378644)
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Project Period (FY) |
2019-04-01 – 2023-03-31
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Keywords | 加齢性難聴 / 内耳性難聴 / 免疫 / 組織マクロファージ |
Outline of Final Research Achievements |
For the purpose of development of novel therapies for hearing loss that target macrophages in the inner ear, there is a need to elucidate their tissue of origin and dynamics. Analysis of the Csf1 signaling pathway in age-related hearing loss suggests that Csf1 signaling is important not only for inner ear bone formation, but also for the maintenance of resident macrophages in the spiral ligament and stria vascularis in adult mouse cochlea. In addition, it was suggested that resident macrophages in the mouse inner ear are supplied and replaced by fetal liver and bone marrow after birth, and that the tissue from which macrophages originate migrates from the yolk sac, fetal liver, or bone marrow. This study provides basic knowledge for the development of therapies targeting resident macrophages in the inner ear to prevent and treat age-related hearing loss in the future.
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Free Research Field |
内耳の免疫学
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Academic Significance and Societal Importance of the Research Achievements |
蝸牛の組織マクロファージは、内耳の恒常性を維持し、内耳の損傷に続いて免疫学的に最前線で防御機構の一部として役割を担うと考えられている。ただし蝸牛組織マクロファージの役割の詳細は知られておらず、今後内耳のマクロファージを標的とした難聴に対する新規治療を開発するにあたり、基盤となる知識としてその由来組織や動態を解明することが求められている。 本研究の実施により、今後の増加の一途を辿る加齢性難聴を予防、治療を見据えて、骨髄由来の内耳組織マクロファージを標的とした新たな治療法を模索するための基礎的な知見が得られた。
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