Role of neutrophil elastase and the endogenous inhibitor elafin in eosinophilic sinusitis

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K11358
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Otorhinolaryngology
• Research Institution: Shiga University of Medical Science
• Principal Investigator: Hideaki Kouzaki 滋賀医科大学, 医学部, 講師 (10402710)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: 好酸球性副鼻腔炎 / エラスターゼ / IL-33

Outline of Final Research Achievements

In the epithelial cells of eosinophilic sinusitis, the expression of elafin, an endogenous protease that suppresses neutrophil elastase, was decreased. Moreover, we found that IL-33 was also induced by stimulation of neutrophil elastase itself. Full-length IL-33 was cleaved by neutrophil elastase, and the cleaved biological activity was found to cause stronger type 2 inflammation than recombinant IL-33.
Failure of elafin's suppression mechanism of neutrophil elastase may contribute to the exacerbation of eosinophilic sinusitis.

Free Research Field

耳鼻咽喉科

Academic Significance and Societal Importance of the Research Achievements

好酸球性副鼻腔炎は難治性疾患であり、ステロイド治療以外の新たな治療が模索されている。本研究では、好中球エラスターゼに着目し、その抑制機能の破綻が好酸球性副鼻腔炎の悪化因子になっていることが推定される実験結果が認められた。