| Project/Area Number |
16K11450
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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 | Nagasaki University |
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Principal Investigator |
SATO Keiko 長崎大学, 医歯薬学総合研究科(歯学系), 助教 (70410579)
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| Co-Investigator(Kenkyū-buntansha) |
今田 勝巳 大阪大学, 理学研究科, 教授 (40346143)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | type IX secretion system / Porphyromonas gingivalis / secretion / Ig-like domain / 歯周病菌 / タンパク質分泌装置 / 病原因子 / 口腔細菌学 |
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| Outline of Final Research Achievements |
The periodontal pathogen Porphyromonas gingivalis secretes many potent virulence factors using the type IX secretion system (T9SS). T9SS cargo proteins are composed of a signal peptide, functional domain(s), an immunoglobulin (Ig)-like domain, and a C-terminal domain.
T9SS cargo proteins were degraded when their Ig-like domains were lacking or truncated. The degradation was dependent on the activity of a quality control factor, HtrA protease. These results suggest that the Ig-like domain mediates stability of the cargo proteins in the T9SS.
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| Academic Significance and Societal Importance of the Research Achievements |
歯周病は心血管疾患、脳梗塞、糖尿病、早産などとの関連性も指摘されている慢性細菌感染症であり、細菌の産生する病原因子により、直接的および間接的に歯周組織の破壊が生じる疾患となる。
細菌のタンパク質分泌は、それらの病原性に関わる。主要な歯周病菌が持つ病原因子分泌装置に関与する研究を行うことで、歯周病細菌の病原性制御に繋がる可能性がある。
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