2017 Fiscal Year Final Research Report
Research for anti-inflammatory therapeutic strategy against pulmonary fibrosis
Project/Area Number |
15K09546
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Collagenous pathology/Allergology
|
Research Institution | Gunma University |
Principal Investigator |
HISADA Takeshi 群馬大学, 医学部附属病院, 講師 (10344938)
|
Co-Investigator(Renkei-kenkyūsha) |
OKAJIMA Fumikazu 青森大学, 薬学部, 教授 (30142748)
|
Research Collaborator |
YATOMI Masakiyo 群馬大学, 医学部附属病院, 助教 (60784105)
SAITO Haruka 群馬大学, 医学部附属病院, 医員 (80447268)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Keywords | 肺線維症 / 脂質メディエーター / resolvin / 炎症収束 / 動物モデル / ω-3脂肪酸 |
Outline of Final Research Achievements |
Pulmonary fibrosis is a destructive inflammatory disease with limited therapeutic options. Resolvin D1 (RvD1) displays potent anti-inflammatory, pro-resolving activity. We tested the hypothesis that 17(R)-RvD1 can provide a therapeutic benefit by reducing inflammation and pulmonary fibrosis. Mice were exposed to bleomycin (BLM) to induce pulmonary fibrosis, and were then treated with 17(R)-RvD1. Administration of 17(R)-RvD1 from the start of BLM treatment attenuated neutrophil alveolar infiltration, lung collagen content, and IL-1β, TGF-β1, CTGF, and type I collagen mRNA expression, along with subsequent reduction in histologically detectable fibrosis. The administration of 17(R)-RvD1 at the later fibrotic stage also improved the lung failure. These results suggest that 17(R)-RvD1 attenuates pulmonary fibrosis by promoting the resolution of neutrophilic inflammation and also provides pulmonary restoration. These data highlight the therapeutic potential of 17(R)-RvD1.
|
Free Research Field |
アレルギー・膠原病
|