| Project/Area Number |
08670677
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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 |
Respiratory organ internal medicine
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| Research Institution | Saitama Medical School |
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Principal Investigator |
MARUO Hitoshi Saitama Medical School, Assistant Professor, 医学部, 講師 (40229604)
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| Co-Investigator(Kenkyū-buntansha) |
TABE Kazuaki Saitama Medical School, Post Doctoral Fellow, 医学部, 助手 (60211372)
NAGATA Makoto Saitama Medical School, Assistant Professor, 医学部, 講師 (20211443)
佐藤 真理 埼玉医科大学, 医学部, 助手 (80275875)
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | eosinophils / H_2O_2 / adhesion molecule / major basic protein / 化学遊走 / 細胞接着 / 活性酸素 / 血管内皮細胞 / VCAM-1 / ロイコトリエンC4 |
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| Research Abstract |
Among inflammatory mediators generated from activated eosinophils, hydrogen peroxide (H_20_2) and leukotriene C4 were examined for their ability to modify eosinophil adhesiveness and expression of endothelial adhesion molecules. 0.1-luM H_20_2significaxitly augmented eosinophil adhesion to endothelial cells. Similar effect was also obtained with luM leukotriene C4. The augmented adhesion with H_20_2activation was blocked by a monoclonal antibody against beta2 integrin, but not by anti- alpha4 antibody. The H_20_2 effect was also partially but significantly inhibited by anti-CD lib antibody, but not by anti-CD11a. H_20_2 enhanced the expression of ODlib and CD18 suggesting that the augmented adhesion occurred, at least in part, via the effects on these adhesion proteins. On the other hand, H_20_2 did modify the expression of VCAM-1 or ICAM-l on endothelial cells. We next asked whether eosinophil major basic protein (MBP) modify the expression of adhesion molecules on eosinophilla. 3uM MBP enhanced the expression of CDIIc and CD54 (ICAM-1). MBP also augmented eosinophil adhesion to endothelial cells. However, the enhanced adhesion was not modified by anti- adhesion molecule antibodies suggesting the involvement of unknown mechanisms in the development of MBP effect.
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