2013 Fiscal Year Final Research Report
The contribution of inflammasome in the pathogenesis of dry eye
| Project/Area Number |
23659816
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Ophthalmology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
SHINOMIYA Katsuhiko 京都府立医科大学, 医学(系)研究科(研究院), 助教 (50585289)
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| Co-Investigator(Kenkyū-buntansha) |
YOKOI Norihiko 京都府立医科大学, 医学研究科, 准教授 (60191491)
UETA Mayumi 同志社大学, 生命医科学部, 准教授 (60398386)
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| Project Period (FY) |
2011 – 2013
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| Keywords | ドライアイ / インフラマゾーム / caspase-1 / ドライアイモデルマウス |
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| Research Abstract |
We developed two dry-eye mouse models induced by exorbital lacrimal gland and intraorbital lacrimal gland excision that could maintain a tear decrease state in a normal breeding environment to investigate the contribution of inflammasome in the pathogenesis of dry eye. We examined interleukin-1 beta (IL-1beta) production in the tear fluid of each model and found that it was increased in the exorbital lacrimal gland excised mice [both wild-type and caspase-1 knock-out (KO)] compared with the untreated controls. The increase of IL-1beta in the tear fluid might suggest that persistent tear-volume reduction could cause some kind of inflammatory reaction on the ocular surface. Of note, the IL-1beta increase in the tear fluid of the caspase-1 KO model was the same as in the wild-type model, suggesting that the IL-1beta production in both models is caspase-1 independent. Our findings suggest that inflammasome is not associated with dry-eye-related inflammation on the ocular surface.
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