| Project/Area Number |
24792335
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Periodontal dentistry
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| Research Institution | Nagasaki University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | インフラマソーム / 歯周炎 / 歯石 / リン酸カルシウム結晶 / 国際情報交換、ドイツ |
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| Outline of Final Research Achievements |
The aim of this study is to investigate whether the crystals in dental calculus could induce activation of NLRP3 inflammasome to produce IL-1β in macrophages and PMNs. WT macrophage incubated with untreated dental calculus produced a robust amount of IL-1β, whereas the cells incubated with heat-treated calculus produced much less IL-1β. After LPS priming, WT macrophage incubated with heat-treated calculus produced considerable level of IL-1β. However, Nlrp3-/- macrophage produced marginal level of IL-1β. Addition of Z-VAD-FMK significantly suppressed the IL-1β production. Similarly, human PMN incubated with heat-treated calculus produced IL-1β. The IL-1β production by PMN was also inhibited by Z-VAD-FMK, indicating involvement of caspase 1.These results indicate that the crystals in dental calculus could accelerate production of IL-1β through NLRP3 inflammasome activation in mouse macrophage and human PMNs.
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