2019 Fiscal Year Final Research Report
Recognition of Candida albicans and mechanism of inflammatory response via HO-1 in oral mucosal cells
Project/Area Number |
17K11841
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Surgical dentistry
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Research Institution | Hiroshima University |
Principal Investigator |
FUKUI AKIKO 広島大学, 病院(歯), 助教 (50647550)
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Co-Investigator(Kenkyū-buntansha) |
太田 耕司 広島大学, 医系科学研究科(歯), 教授 (20335681)
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Project Period (FY) |
2017-04-01 – 2020-03-31
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Keywords | Heme oxygenase 1 / ROS / CEACAM1 / Candida albicans / 口腔粘膜上皮細胞 / 炎症性サイトカイン |
Outline of Final Research Achievements |
We investigated the mechanism of inflammatory response to Ca in oral keratinocyte. In this study, we found that Ca induced HO-1 expression via ROS in oral keratinocyte and it was revealed that HO-1 controlled inflammatory cytokines which induced by Ca β-glucan. Recently CEACAM1 was recognized as a Ca receptor, we investigated its function to Ca in oral keratinocyte. CEACAM1 was expressed and localized in the cell membrane of RT7, and its expression was increased by heat-killed Ca and Caβ-glucan.HO-1 expression which induced by Ca was decreased in CEACAM1 SiRNA. Therefore, CEACAM1 recognizes Ca in the oral keratinocyte and it induced HO-1 expression via ROS.
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Free Research Field |
口腔外科
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Academic Significance and Societal Importance of the Research Achievements |
口腔カンジダ症は常在菌であるCandida albicansが主な原因菌の感染症で,有病者や高齢者など免疫力の低下した状態や,唾液の減少・長期の抗菌薬使用による常在菌間のバランスの乱れにより病原性を発揮し発症するとされる。口腔粘膜は細菌やウイルスが最初に接する器官で,病原菌に対する防御機構が存在すると考えられるが,口腔粘膜細胞におけるCaの認識機構や免疫応答については不明な点が多い。これらを解明することで既存の抗真菌薬と異なる経路をターゲットにした新規治療薬の開発や,易感染患者の口腔内の炎症制御,深在性カンジダ症など重症例の防止につながり,有病者のQOL向上に貢献することができる分野である。
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