| Project/Area Number |
17K11627
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Showa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
深町 はるか 昭和大学, 歯学部, 助教 (10433799)
桑田 啓貴 昭和大学, 歯学部, 教授 (60380523)
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| Project Period (FY) |
2017-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | Streptococcus sanguinis / csRNA / Streptococcus oralis / 細菌 / 核酸 / 感染症 |
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| Outline of Final Research Achievements |
We targeted Streptococcus sanguinis, which is the main causative agent of infective endocarditis, and analyzed the regulatory mechanism of pathogenicity of the bacteria, focusing on small RNA (sRNA). We constructed a strain lacking csRNA, which is a type of sRNA of S. sanguinis, to examine the function of csRNA, and it became clear that the expression of pilT, which is one of the genes constituting the type IV pili operon, is suppressed by csRNA. Furthermore, the biofilm-forming ability was increased in the csRNA-deficient strain. These results suggest that the csRNA of S. sanguinis may regulate pilT in response to the changes in the external environment and regulate the expression of pathogenicity of the bacteria.
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| Academic Significance and Societal Importance of the Research Achievements |
近年、様々な薬剤耐性菌の増加が報告されており、新たな感染症治療法の開発は重要な課題である。しかし、従来の病原菌の殺滅を目的とするような方法では耐性菌の出現は避けられず、新たな視点に立った治療法の開発が必要である。本研究は細菌の排除ではなく病原性の発現を抑制する方法の開発を目指し、細菌の病原性発現機構の解析を行った。口腔常在菌の一種で、血流中では病原性を発揮するStreptococcus sanguinisにおける解析の結果、低分子RNAが病原性の発現に重要な働きをすることが明らかとなった。この研究成果は低分子RNAを標的とした新たな感染症治療法の開発の基盤となり、きわめて意義深いと考えられる。
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