2016 Fiscal Year Final Research Report
Evaluation of autoinflammatory responses in mouse cochlea
| Project/Area Number |
15H06255
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Otorhinolaryngology
|
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
|
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| Project Period (FY) |
2015-08-28 – 2017-03-31
|
| Keywords | 蝸牛 / 免疫応答 |
|---|
| Outline of Final Research Achievements |
NLRP3 protein is expressed in innate immune cells including macrophages. Gain of function mutations of NLRP3 induce the activation of NLRP3 inflammasome, resulting in the secretion of proinflammatory cytokine, interleukin-1 beta, to cause systemic inflammatory diseases, cryopyrin associated periodic syndromes. We found that a gain of function mutation of NLRP3 also caused non-syndromic hearing loss. We hypothesized that the hearing loss was caused by the activation of NLRP3 inflammasome mainly in the cochleae. We revealed that tissue-resident macrophage-like cells existed and mRNAs consisting NLRP3 inflammasome were expressed in the wild type mouse cochleae.
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| Free Research Field |
耳鼻咽喉科学
|
