| Project/Area Number |
15K21190
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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 |
Respiratory organ internal medicine
Experimental pathology
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| Research Institution | Hiroshima University |
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Principal Investigator |
Nakashima Taku 広島大学, 病院(医), 病院助教 (90643792)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 肺障害 / 骨髄移植 / B7Hファミリー / 肺線維症 / 記憶免疫 / ブレオマイシン |
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| Outline of Final Research Achievements |
To clarify the mechanism of drug-induced lung injury (DILD), we hypothesize that the lung response to an initial insult, such as bleomycin (BLM) treatment, alters the phenotype of bone marrow (BM) cells such that they will contribute to exacerbation of DILD. Cells from BM of control or BLM-treated donor mice were transplanted into naive recipient mice. Upon BLM treatment recipient mice transplanted with BM from BLM-pretreated donors showed significant exacerbation of fibrosis relative to mice receiving BM from controls. Moreover B7H3 positive cell numbers were solely upregulated among analyzed B7 family molecules. These effects were also noted in BLM-treated mice that were pretreated with a suboptimal dose of BLM, but were abolished if the mice were transplanted with BM from naive mice. These results suggested that B7H3 played a role in the pathophysiology of DILD.
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