The parthenogenesis of eosinophilic chronic rhinosinusitis

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K11207
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Otorhinolaryngology
• Research Institution: University of Fukui
• Principal Investigator: Takabayashi Tetsuji 福井大学, 学術研究院医学系部門(附属病院部), 講師 (70397272)
• Co-Investigator(Kenkyū-buntansha): 加藤 幸宣 福井大学, 学術研究院医学系部門(附属病院部), 助教 (00748981) ; 坂下 雅文 福井大学, 学術研究院医学系部門(附属病院部), 講師 (40555455)
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 好酸球性副鼻腔炎 / 鼻茸 / アスピリン喘息

Outline of Final Research Achievements

Nasal polyps from patients with aspirin-exacerbated respiratory disease (AERD) are defines by a predominant Th2 inflammation environment. L-plastin protein levels in nasal polyp tissue were increased in patients with AERD relative to those in patients with aspirin tolerant CRSwNP. Immunofluorescence analysis revealed that L-plastin was dominantly expressed in eosinophils and L-plastin and TF were co-expressed in eosinophils in AERD nasal polyp tissue. Silencing of L-plastin in Eol-1 cells disrupted the cell surface distribution of TF by stimulation with granulocyte macrophage colony-stimulating factor. The expression of L-plastin by eosinophils may contribute to abnormal fibrin deposition through TF translocation to the eosinophil cell surface in AERD nasal polyp tissue, which in turn may contribute to the pathogenesis of AERD.

Free Research Field

耳鼻咽喉科・頭頸部外科

Academic Significance and Societal Importance of the Research Achievements

好酸球性副鼻腔炎は非常に難治性の疾患で厚生労働省によって指定難病に登録されている。本疾患において最重症タイプのアスピリン喘息における鼻茸形成のメカニズムについてはこれまであまり分かっていなかった。今回の研究結果によって好酸球性副鼻腔炎における鼻茸形成メカニズムが解明され今後新規治療法の開発にも大きく役立つと思われる。