2014 Fiscal Year Final Research Report
Elucidation of mechanisms by which cimetidine prevents febrile attacks of PFAPA syndrome
| Project/Area Number |
24591564
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | University of Occupational and Environmental Health, Japan |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SATO Tetsuji 産業医科大学, 医学部, 助教 (10389447)
SATO Kaoru 産業医科大学, 医学部, 助教→非常勤医師 (70596733)
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| Co-Investigator(Renkei-kenkyūsha) |
KAMIZONO Junji 産業医科大学, 医学部, 非常勤医師 (50299616)
MIYAKAWA Takayuki 産業医科大学, 医学部, 非常勤医師 (90219733)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 周期性発熱 / PFAPA症候群 / 自己炎症疾患 / シメチジン / 治療 / 作用機序 |
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| Outline of Final Research Achievements |
In analyses using cDNA microarray and quantitative RT-PCR of peripheral blood mononuclear cells (PBMCs), regulator of G-protein signaling 1 (RGS1)showed higher expression in PFAPA patients without cimetidine medication than in normal controls and lower expression in PFAPA patients with cimetidine medication than those without. It was suggested that reduced expression of RGS1 in PBMCs played an important role in cimetidine-induced inhibition of inflammatory response. Furthermore, comparison of LPS-added monocytoid leukemia cell line, THP-1 culture and LPS plus cimetidine-added THP-1 culture using the same analytical strategy, we demonstrated reduced expression of IL-10 in LPS plus cimetidine-added THP-1 culture, suggesting that reduced expression of IL-10 in monocytes was also associated with cimetidine-induced inhibition of inflammatory response.
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| Free Research Field |
小児感染症学、自己炎症疾患
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