Analysis of the inflammatory mechanism in host-parasite relationship through inflammasome activity
| Project/Area Number |
25861775
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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 |
Pathobiological dentistry/Dental radiology
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| Research Institution | Kyushu Dental College |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | インフラマソーム / 歯周病細菌 / 炎症性サイトカイン / 宿主寄生体相互関係 / マクロファージ / ピロトーシス / 自然免疫 |
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| Outline of Final Research Achievements |
In the present study, the periodontopathic bacterial pathogen, Aggregatibacter actinomycetemcomitans, induced cell death and cytokine release in macrophages. Pattern recognition receptor, NLRP3 was upregulated in A. actinomycetemcomitans-invaded macrophages. However, NLRP3 knockdown had no effect on the secretion of IL-1β in A. actinomycetemcomitans-invaded RAW 264 cells. A. actinomycetemcomitans invasion induced the generation of reactive oxygen species (ROS) and the release of cathepsin B in RAW 264 cells. CA074-Me, a cathepsin B inhibitor, and N-Acetyl-L-cysteine (NAC), a ROS inhibitor, prevented the production of IL-1β induced by A. actinomycetemcomitans. Taken together, these results suggest A. actinomycetemcomitans induce IL-1β production in RAW 264 cells through the production of ROS and cathepsin B, but not through the NLRP3/caspase-1 pathway.
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Report
(3 results)
Research Products
(8 results)
