The pathology of eosinophilic chronic rhinosinusitis focused on eosinophil-fibroblast interactions.
Project/Area Number |
15K20200
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Otorhinolaryngology
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Research Institution | Shiga University of Medical Science |
Principal Investigator |
|
Research Collaborator |
Shimizu Shino
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 好酸球性副鼻腔炎 / 線維芽細胞 / 好酸球 / 凝固因子 / EGF受容体阻害薬 / eotaxin-1 / RANTES / トロンビン / フィブリン |
Outline of Final Research Achievements |
Eosinophilic chronic rhinosinusitis (ECRS) is a refractory upper airway disease, characterized by significant eosinophil infiltration, glue-like rhinorrhea and recurrent nasal polyposis. In the present study, we found that eosinophil-fibroblast interactions promoted infiltration of inflammatory cell such as neutrophil and eosinophil. We also elucidated that tissue factor expression by eosinophil activated coagulation cascade, and coagulation factors stimulated nasal mucosa fibroblasts via protease-activated receptors (PARs). As a result, deposition of extracellular matrix and eosinophil infiltration induced. Intranasal instillation of EGFR tyrosine kinase suppressed eosinophil infiltration and goblet cell metaplasia in ovalbumin (OVA)-induced allergic inflammation of rat nose. The results indicate that local administration of EGFR inhibitor may provide a new therapeutic potential for the treatment of intractable airway diseases such as ECRS.
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Report
(4 results)
Research Products
(2 results)