| Project/Area Number |
25861571
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Oita University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 遺伝子改変マウス / SOCS遺伝子 / アレルギー性鼻炎 / 中耳炎 / SOCS |
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| Outline of Final Research Achievements |
Suppressor of cytokine signaling (SOCS) is a negative feedback regulator of IL-4-dependent pathways and might therefore control Th2 immunity associated traits, such as IgE levels and eosinophilic mucosal inflammation, which are implicated in allergic rhinitis. Otitis media and allergic rhinitis is thought to be strongly correlated each other in clinic. To confirm the relationship between these two disease, SOCS1 knockout mice was used as a model of allergic rhinitis, and then artificially caused otitis media. The mucosa of SOCS1 group mice was seen much higher infiltration with eosinophils and inflammation cells. In multiplex ELISA of middle ear washing fluid, many cytokines, not only Th2 but also Th1, were more stimulated in SOCS1 group than control. Th2 type cytokines were thought to be related to allergy, but Th1 type cytokines were also induced by allergic rhinitis. This result may be milestone to improve the treatment against otitis media combined with allergic rhinitis.
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