Involvement of bone marrow-derived fibrocyte in the pathogenesis of pulmonary fibrosis and the effect of newly developed anti-fibrotic agents
Project/Area Number |
23591163
|
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 |
AZUMA Arata 日本医科大学, 医学部, 教授 (10184194)
|
Co-Investigator(Kenkyū-buntansha) |
神尾 孝一郎 日本医科大学, 医学部, 助教 (20465305)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | 特発性肺線維症 / 線維細胞 / ピルフェニドン / fibrocyte |
Research Abstract |
Bone marrow-derived fibrocytes reportedly play important roles in the pathogenesis of idiopathic pulmonary fibrosis. Pirfenidone (PFD) is an anti-fibrotic agent; however, its effects on fibrocytes have not been investigated. The aim of this study was to investigate whether PFD inhibits fibrocyte pool size in the lungs of bleomycin (BLM)-treated mice. To achieve this, C57BL/6 mice were treated with BLM and PFD was administered. Fibrocyte pool size in BLM-treated mice lungs was attenuated by PFD. This was also observed in a therapeutic setting. Increased chemokine (CC motif) ligand-2 (CCL2) and CCL12 production in BLM-treated mouse lungs was significantly attenuated by PFD. Fibrocyte migration toward CCL2 and chemokine (CC motif) receptor-2 expression on fibrocytes were significantly inhibited by PFD in vitro. Fibrocyte inhibition is considered a mechanism of anti-fibrotic action of PFD.
|
Report
(4 results)
Research Products
(7 results)