2015 Fiscal Year Final Research Report
Pathologic Analysis of Intractable Chronic Rhinosinusitis Based on Epigenetic Mechanisms
| Project/Area Number |
24592582
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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 |
Otorhinolaryngology
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| Research Institution | Toho University |
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Principal Investigator |
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| Research Collaborator |
MATSUMOTO Kenji 国立成育医療研究センター, 免疫アレルギー・感染研究部, 部長 (60181765)
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Keywords | 慢性副鼻腔炎 / 気管支喘息 / ウイルス感染 / 線維芽細胞 / エピゲノム制御機構 |
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| Outline of Final Research Achievements |
Chronic rhinosinusitis (CRS) is characterized by local inflammation of the sinonasal tissues. CRS patients with nasal polyps and asthma often develop acute exacerbation of sinonasal symptoms after upper respiratory tract infections. Nasal fibroblasts isolated from the specimens were stimulated with poly I:C. CXCL10 expression was analyzed. Biopsy specimens were subjected to immunohistochemistry for detection of T-bet and GATA-3 expression in CD3+ T cells by double labeling. Nasal fibroblasts from the aspirin-tolerant asthma (ATA) and aspirin-intolerant asthma (AIA) patients showed significantly enhanced expression of CXCL10 mRNA and protein after poly I:C stimulation. In addition to T helper (Th)2 cells, there was more abundant infiltration of Th1 cells into tissues from the AIA and ATA patients. Our findings suggest that CRS associated with asthma may become intractable through the over-production of CXCL10 in response to viral infection.
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| Free Research Field |
耳鼻咽喉科学
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