| Project/Area Number |
15K11430
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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 |
Social dentistry
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| Research Institution | Nihon University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
SHIMIZU Kazufumi 神戸大学, 大学院医学研究科, 客員教授 (50004677)
IMAI Kenichi 日本大学, 歯学部, 教授 (60381810)
TAMURA Muneaki 日本大学, 歯学部, 准教授 (30227293)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | インフルエンザウイルス / 口腔細菌 / ジンジパイン / Porphyromonas gingivalis |
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| Outline of Final Research Achievements |
During the initial critical steps in influenza A virus (IAV) infection, cleavage of the viral hemagglutinin (HA) by trypsin-like protease is required for expression of fusion activity and virus entry into cells. Porphyromonas gingivalis produces trypsin-like proteases, such as arginine-gingipain (Rgp) and lysine-gingipain (Kgp). We found that P. gingivalis culture supernatants had the ability to cleave HA, thereby, contribute to induction of viral infection. Moreover, we also demonstrated that Rgp inhibitor suppressed HA cleavage and infected cells via P. gingivalis culture supernatants. In addition, the culture supernatants of P. gingivalis Rgp-null mutant and Rgp/Kgp-null mutant were not able to cleave HA, thereby, inhibit the spread of IAV infection. In contrast, culture supernatants of wild-type and Kgp-null mutant activated infectivity IAV through HA proteolytic cleavage. Taken together, these results suggest that Rgp has the ability to cleave HA and contribute to viral spread.
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