| Project/Area Number |
23591154
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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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 |
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| Co-Investigator(Renkei-kenkyūsha) |
KUROKI Yoshio 札幌医科大学, 医学部, 教授 (70161784)
SHIRATORI Masanori 札幌医科大学, 医学部, 准教授 (40295366)
CHIBA Hirofumi 札幌医科大学, 医学部, 講師 (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) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 急性肺障害 / ブレオマイシン / 肺コレクチン / 肺サーファクタントタンパク質A / トル様受容体 / 薬剤性肺障害 / Toll-like receptor |
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| Research Abstract |
The purpose of this project were to clarify the mechanism of regulation by which Toll-like receptors (TLRs) act against drug-induced acute lung injury (ALI), to evaluate the protective effect by lung a collectin, SP-A and to establish the molecular basis for the clinical application of it. Bleomycin (BLM)-administered SP-A(-/-) mice had significantly higher mortality rate and more increase of inflammatory cytokines in the lungs than wild types. SP-A inhibited BLM-induced inflammatory cytokines from rat alveolar macrophages. sTLR2 gene-transfected HEK293 cells showed up-regulation of NF-kB. BML bound directly with sTLR2 and its binding was blocked by SP-A. These results indicate that BLM-induced signal depends on TLR2 and lung collectin, SP-A has protective function against ALI via TLR2 dependent signal pathway.
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