Project/Area Number |
26461201
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Respiratory organ internal medicine
|
Research Institution | Nippon Medical School |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
吾妻 安良太 日本医科大学, 医学部, 教授 (10184194)
|
Research Collaborator |
MATSUDA Kuniko 日本医科大学, 実験助手
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 制御性T細胞 / 特発性肺線維症 / ブレオマイシン / FGF9 / IL-10 / 自家骨髄細胞 / 再生医療 |
Outline of Final Research Achievements |
In the current study, we aimed at the resolution of pulmonary fibrosis using autologous bone marrow or spleen cells. Pulmonary fibrosis was induced by bleomycin (BLM) (day 0), then, bone marrow cells or spleen cells were adoptively transferred via tail veins on day 7 or 14. Adoptive transfer of spleen cells significantly ameliorated BLM-induced murine pulmonary fibrosis on day14. This effect was abrogated by neutralization of CD25 by anti-CD25 monoclonal antibody, which suggests that regulatory T cells (Tregs) are involved in the effect of spleen cells. To further characterize the mechanisms by which Tregs exert anti-fibrotic effects, we isolated Tregs from spleens of C57BL/6 mice using magnetic beads, then, adoptively transferred them into BLM-induced pulmonary fibrosis mice on day 14. Tregs significantly ameliorated pulmonary fibrosis which was measured by Ashcroft score and hydroxyproline. This was accompanied by reduced expression of fibroblast growth factor 9 and IL-10.
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