| Project/Area Number |
20591197
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
膠原病・アレルギー・感染症内科学
|
|---|
| Research Institution | Department of Clinical Research, National Hospital Organization Nagasaki Medical Center |
|---|
Principal Investigator |
MIGITA Kiyoshi Department of Clinical Research, National Hospital Organization Nagasaki Medical Center, 臨床研究センター, 病因解析研究部長 (60264214)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
ISHIBASHI Hiromi 独立行政法人国立病院機構長崎医療センター, 臨床研究センター, センター長 (80127969)
EGUCHI Katumi 長崎大学, 医歯薬学総合研究科, 教授 (30128160)
石橋 大海 独立行政法人国立病院機構(長崎医療センター臨床研究センター), 臨床研究センター長 (80127696)
|
|---|
| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Keywords | ryopyrin / 自己炎症性疾患 / 家族性地中海熱 / 関節リウマチ / 血清アミロイドA蛋白 / Cryopyrin / cropyrin / MEFV遺伝子 / Pyrin / cryopyrin / pyrin / MEFV / アミロイドーシス |
|---|
| Research Abstract |
The mechanism by which inflammasome activation and following IL-1β induction in autoinflammation is not completely elucidated. We studied the role of serum amyloid A (SAA) in the regulation of IL-1β production and activation of inflammasome cascade in human rheumatoid synoviocytes. Rheumatoid synoviocytes stimulated with SAA express NLRP3 (cryopyrin) mRAN expression. MSU (modosodium urate), a ligand for NLRP3, stimulation did not induce IL-1β production in rheumatoid synoviocytes. Whereas, rheumatoid synoviocytes pretreated with low concentration (1-5μg/ml) of SAA produce IL-1β in response to MSU. These findings indicate that during systemic inflammation, SAA may promote the MSU-induced IL-1β induction through activating the NLRP3 inflammasome activation.
|
