| Project/Area Number |
18591132
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
膠原病・アレルギー・感染症内科学
|
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| Research Institution | Clinical research Center, Chiba-East National Hospital, National Hospital Organization |
|---|
Principal Investigator |
RYUTARO Matsumura Clinical research Center, Chiba-East National Hospital, National Hospital Organization, Division of clinical immunology, Clinical Research Center of Chiba east, 部長 (70246742)
|
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| Project Period (FY) |
2006 – 2007
|
| Project Status |
Completed (Fiscal Year 2007)
|
| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥330,000)
Fiscal Year 2007: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2006: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | galectin-3 / pulmonary fibrosis / lectin / 肺線維症 |
|---|
| Research Abstract |
Galectin-3 was specifically increased in BALF from patients with pulmonary fibrosis (IPF) and interstitial pneumonia associated with collagen vascular disease (CVD-IP). Galectin-3 levels in BALF seemed to be lower in IPF and CVD-IP patients receiving corticosteroid therapy. Alveolar macrophages from IPF patients expressed more galectin-3 compared with those from control. Galectin -3 expression was induced by tumor necrosis factor-alpha (TNF-a) and interferon (IFN)-r in a macrophage cell line U937. Galectin -3 also induced mRNA expression and protein production of TNF-a and interleukin (IL) -8 in a macrophage cell line THP-1. This lectin stimulated NIH-3T3 fibroblast to induce migration and collagen synthesis in vitro. These results suggest that Galectin-3 is involved in the pathogenesis fo human IPF and CVD-IP by activating macrophages and fibroblasts.
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