| Project/Area Number |
18K17027
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 57020:Oral pathobiological science-related
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| Research Institution | Osaka University |
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Principal Investigator |
Ogawa Mariko 大阪大学, 歯学研究科, 招へい教員 (20754732)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | インフルエンザウイルス / 肺炎球菌 / 肺炎 / インフルエンザ / レンサ球菌 / 重複感染 |
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| Outline of Final Research Achievements |
Influenza infection predisposes the host to secondary bacterial pneumonia, a major cause of mortality during influenza epidemics. Here, we found that epithelial cells in humans infected with the influenza A virus (IAV) exhibit GP96 on the cell surface, an endoplasmic reticulum chaperon for numerous cell surface and secreted proteins. The present findings showed that Streptococcus pneumoniae demonstrated a greater level of efficient adherence to IAV-infected alveolar epithelial cells as compared to non-infected cells, while that enhanced bacterial association was reduced by introduction of a pharmacological GP96 inhibitor.
Together, our results offer insight regarding the mechanism for IAV-induced redistribution of GP96 on epithelial surfaces, which plays a critical role in secondary pneumococcal infection.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では，ウイルスと細菌が重複感染した宿主における複雑な病態形成機構を明らかにし，既存の治療法に代わる感染制御法の提案を目的として推進した．A型インフルエンザウイルス感染により気道上皮細胞に表出したGP96は細菌に対する宿主レセプターとして機能するが，GP96抑制剤の添加によりウイルス感染細胞への細菌の付着は抑制されることを証明した．したがって，ウイルス感染に伴い表在化するGP96は有効な感染防御標的分子であり，インフルエンザに重複する細菌性肺炎の新規感染制御法の開発に応用できると考える．
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