| Project/Area Number |
25860824
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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 |
Infectious disease medicine
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| Research Institution | Hokkaido University |
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Principal Investigator |
MATSUO Junji 北海道大学, 大学院保健科学研究院, 講師 (50359486)
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 肺炎クラミジア / カーボンナノ粒子 / IL－１β / カーボンナノチューブ / IL-1 |
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| Outline of Final Research Achievements |
We investigated whether Chlamydia pneumoniae stimulation with carbon nanoparticles synergistically enhance proinflammatory cytokine IL-1β from macrophages. Carbon nanotubes were used as carbon nanoparticles. As a result, although mature IL-1β was detected in the supernatants of C. pneumoniae-stimulated macrophages, the synergistic stimulation of the cells by C. pneumoniae and carbon nanotubes clearly increased the IL-1β secretion. TEM observation revealed co-localization of C. pneumoniae and carbon nanotubes in a macrophage. Carbon nanotube stimulation did not induce the IL-1β mRNA expression. Actin polymerization inhibitor and caspase inhibitors blocked IL-1β secretion. In addition, IL-1β secretion was decreased in NLRP3 KD cells, suggesting that phagocytosis of carbon nanotubes enhances pro-IL-1β cleavage through NLRP3 inflammasome activation. Thus, the results imply that carbon nanoparticles may have a significant impact in exacerbations of C. pneumoniae infection.
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