| Project/Area Number |
15209029
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (A)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Respiratory organ internal medicine
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
NAGASE Takahide The University of Tokyo, Faculty of Medicine, Professor, 医学部附属病院, 教授 (40208004)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
KURIHARA Hiroki The University of Tokyo, Graduate School of Medicine, Professor, 大学院医学系研究科, 教授 (20221947)
清水 孝雄 東京大学, 大学院・医学系研究科, 教授 (80127092)
|
|---|
| Project Period (FY) |
2003 – 2006
|
| Project Status |
Completed (Fiscal Year 2006)
|
| Budget Amount *help |
¥48,100,000 (Direct Cost: ¥37,000,000、Indirect Cost: ¥11,100,000)
Fiscal Year 2006: ¥11,050,000 (Direct Cost: ¥8,500,000、Indirect Cost: ¥2,550,000)
Fiscal Year 2005: ¥11,050,000 (Direct Cost: ¥8,500,000、Indirect Cost: ¥2,550,000)
Fiscal Year 2004: ¥11,050,000 (Direct Cost: ¥8,500,000、Indirect Cost: ¥2,550,000)
Fiscal Year 2003: ¥14,950,000 (Direct Cost: ¥11,500,000、Indirect Cost: ¥3,450,000)
|
|---|
| Keywords | Lipid mediators / Antimicrobial peptides / Transgenic mouse / Knockout mouse |
|---|
| Research Abstract |
Inflammatory lung diseases including acute lung injury and pulmonary fibrosis are of significant importance in terms of both motality and difficulty in management. Acute respiratory distress syndrome (ARDS) is an acute lung injury and the mortality rate for ARDS ranges from 40-70% despite of intensive care. Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal disorder of the lung parenchyma, while no useful drugs are currently available to treat IPF. However, molecular mechanisms underlying these lung diseases are little known and the development of a novel therapeutic strategy is of urgent necessity. The purpose of this project is to investigate molecular mechanisms underlying inflammatory lung diseases and develop novel therapeutic strategies. We studied the pathophysiological roles of 1) lipid mediators including platelet-activating factor (PAF) and metabolites of arachidonic acid, i.e., eicosanoids, 2) CGRP family peptides, and 3) antimicrobial peptides. We have shown that these substances might be involved in the pathogenesis of inflammatory lung diseases including ARDS and IPF, suggesting that bioactive mediators, e.g., lipid mediators, might be potential targets to develop a novel therapeutic strategy to refractory lung diseases.
|
