| Project/Area Number |
21390197
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Hygiene
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| Research Institution | Kitasato University (2010-2011)
National Institute for Environmental Studies (2009) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SONE Yuka 北里大学, 薬学部, 助教 (60550035)
柳澤 利枝 独立行政法人国立環境研究所, 環現健康研究領域, 主任研究員 (70391167)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥14,430,000 (Direct Cost: ¥11,100,000、Indirect Cost: ¥3,330,000)
Fiscal Year 2011: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2009: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
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| Keywords | 環境保健 |
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| Research Abstract |
In reality, we inhale suspended DEP and/or nanoparticles in ambient air Nevertheless, assessment of the impact of inhalation/intratracheal exposure to diesel engine-derived nanoparticles, a more realistic exposure, on the lung inflammation model has never been conducted. Furthermore, as far as we know, no study has examined the dose-dependent effects of inhaled nanoparticles on predisposed subjects. The present study investigated the impact of pulmonary exposure to diesel-engine-derived nanoparticles on emphysematous lung injury and allergic airway inflammation and dissolved its underlying mechanisms. In the first experiments, CBNP of 14 nm significantly induced acute lung inflammation in non-elicited subjects, and aggravated PPE-elicited airway neutrophilic inflammation at an early stage, which was concomitant with the enhanced lung expression of proinflammatory cytokines. In the next experiments, high concentration of NR-DE significantly deteriorated OVA-induced eosinophilic airway inflammation. On the other hand, DE gas did not influence PPE-induced pulmonary inflammation with emphysema. In in vitro experiments, NR-DEP significantly enhanced mucin-1 expression on BEAS-2B cells and surface expression of CD86 on mouse-derived splenocytes and dendritic cells.
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