2016 Fiscal Year Final Research Report
Endogenous protease inhibitor in airway epithelial cells contribute to eosinophilic chronic rhinosinusitis
| Project/Area Number |
26462582
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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 | Shiga University of Medical Science |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | プロテアーゼ / サイトカイン / 好酸球性副鼻腔炎 / 上皮細胞 / 内因性プロテアーゼインヒビター |
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| Outline of Final Research Achievements |
Cystatin A and SPINK5 are endogenous protease inhibitors (EPIs) that may play key roles in epithelial barrier function. The purpose of this study was to investigate the roles of EPIs in the pathogenesis of chronic rhinosinusitis (CRS).
Thw patients with eosinophilic CRS showed lower protein and mRNA expression of cystatin A and SPINK5 in the nasal epithelium. Allergen-induced production of IL-25, IL-33, and TSLP in normal human bronchial epithelial cells was mediated by treatment with recombinant cystatin A or SPINK5. Chronic MAA exposure induced epithelial disruption in mouse nasal epithelium and decreased the tissue expression and nasal lavage levels of cystatin A and SPINK5. Intranasal instillations of recombinant EPIs attenuated this MAA-induced pathology.
Cystatin A and SPINK5 play an important role in protecting the airway epithelium from exogenous proteases. The preservation of EPIs may have a therapeutic benefit in intractable airway inflammation such as eosinophilic CRS.
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| Free Research Field |
医歯薬学
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