2013 Fiscal Year Final Research Report
Study of biomarker and pathophysiology in non-hereditary periodic fever syndrome
| Project/Area Number |
23591559
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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 |
SATO Tetsuji 産業医科大学, 医学部, 助教 (10389447)
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| Co-Investigator(Kenkyū-buntansha) |
KUSUHARA Koichi 産業医科大学, 医学部, 教授 (20243941)
SATO Kaoru 産業医科大学, 医学部, 助教 (70596733)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 小児免疫・アレルギー・膠原病学 / 周期性発熱症候群 |
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| Research Abstract |
Febrile period of PFAPA syndrome showed increased mRNA expression of CXCL10, ANKRD22, SERPING1, SLAMF8, GBP1 by microarray and quantitative RT-PCR, compared to non-febrile period of PFAPA syndrome, normal controls and disease controls. In quantification of inflammatory markers, CD64 expression on monocytes was increased in febrile period of PFAPA syndrome. Serum level of CXCL9, a monocyte-derived chemokine, was higher in febrile period of PFAPA syndrome than in adenovirus infection. As these findings suggested that activation of monocytes plays important role in the pathophysiology of PFAPA syndrome, in vitro assay using THP-1 cells, a monocytic leukemia cell line, was performed. Quantitative RT-PCR of THP-1 cells showed increased expression of CXCL10 and GBP1 after stimulation by LPS, suggesting that these molecules play pivotal role in innate immune response of monocytes in PFAPA syndrome.
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