| Project/Area Number |
20590930
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
TAKAHASHI Hiroki Sapporo Medical University, 医学部, 教授 (60231396)
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| Co-Investigator(Kenkyū-buntansha) |
KUROKI Yoshio 札幌医科大学, 医学部, 教授 (70161784)
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| Co-Investigator(Renkei-kenkyūsha) |
SHIRATORI Masanori 札幌医科大学, 医学部, 講師 (40295366)
CHIBA Hirofumi 札幌医科大学, 医学部, 助教 (40347175)
KUDO Kazumi 札幌医科大学, 医学部, 助教 (90438002)
KURONUMA Koji 札幌医科大学, 医学部, 助教 (40563250)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2008: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 薬剤性肺障害 / ブレオマイシン / 肺コレクチン / 肺サーファクタント蛋白質A / トル様受容体 / SP-A / TLR2 / ノックアウトマウス / 肺線維化 |
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| Research Abstract |
The purposes of this project were to investigate the mechanisms of regulation by which lung collectins, surfactant proteins A and D (SP-A and SP-D), and Toll-like receptor (TLR) function against inflammation on the development of drug induced lung injury, and to establish the molecular basis for the clinical application of these proteins. First, the mouse model of lung injury was established using drugs, and SP-A^<-/-> mice had significantly higher mortality rates than WT mice. SP-A inhibited drug-induced inflammatory cytokine production from rat alveolar macrophages. SP-A blocked sTLR2-bleomycin binding in the dose dependent manner. These results suggest that bleomycin signals are transmitted through TLR2 dependent pathway and regulated by the molecular interaction of SP-A.
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