| Project/Area Number |
24791004
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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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 | Saitama Medical University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | danger signal / 尿酸 / ATP / 好酸球 / 好酸球性肺炎 |
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| Research Abstract |
The damaged cell produces danger signal. Danger signal causes influence for inflammation and immunoreaction.There are endogenous danger signal uric acid and ATP.
The ATP induced an eosinophilic migration. The uric acid derived eosinophilic adhesion ability, and the possibility that a part of the reaction went through ATP was suggested. The eosinophilic active oxygen production is derived and is increased in ATP, uric acid stimulation additively in rh-ICAM-1. The eosinophilic cytokine production is derived with ATP. Uric acid, the ATP is produced the lungs in acidophile-related pneumonia locally.
The cell injury may cause eosinophilic accumulation and activity locally.
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