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2015 Fiscal Year Final Research Report

Treatment strategy for intractable upper airway diseases concerning gene-polymorphism-related molecules and local basophils.

Research Project

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Project/Area Number 25293348
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypePartial Multi-year Fund
Section一般
Research Field Otorhinolaryngology
Research InstitutionUniversity of Fukui

Principal Investigator

Takechiyo Yamada  福井大学, 医学部, 准教授 (70283182)

Co-Investigator(Kenkyū-buntansha) SAKASHITA Masafumi  福井大学, 医学部, 助教 (40555455)
IMOTO Yoshimasa  福井大学, 医学部附属病院, 助教 (50418703)
TOMITA Kaori  福井大学, 医学部, 特別研究員 (30444227)
TAKABAYASHI Tetsuji  福井大学, 医学部附属病院, 講師 (70397272)
FUJIEDA Shigeharu  福井大学, 医学部, 教授 (30238539)
Project Period (FY) 2013-04-01 – 2016-03-31
Keywords好塩基球 / 花粉症 / 好酸球性副鼻腔炎 / 好酸球 / 肥満細胞 / 気管支喘息
Outline of Final Research Achievements

The intractable upper airway diseases including Japanese Cedar Pollinosis and eosinophilic chronic rhinosinusitis have been focused on. We have identified the phenotype of pollinosis refractory to sublingual immunotherapy. The antigen-induced expression level of CD203c on basophils from the patients with pollinosis was a more objective and reliable biomarker. The antigen- induced production of IL-4 increased in the basophilic cell line that was over-expressed by the gene-polymorphism-related molecules ORMDL3. Dectin-1 recognizes β-glucan, and dectin-1-mediated signaling stimulated gene expression of IL-4 through Syk in the basophilic cell line. Chronic rhinosinusitis without nasal polyps had increased levels of type 2 mediators, including IL-5, IL-13, eotaxin-2, and MCP-4. Aspirin-exacerbated respiratory disease had elevated protein levels of ECP, GM-CSF, and MCP-1, as well as decreased tissue plasminogen activator.

Free Research Field

耳鼻咽喉科

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Published: 2017-05-10  

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