| Project/Area Number |
17K11840
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
Ohta Kouji 広島大学, 医系科学研究科(歯), 教授 (20335681)
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| Co-Investigator(Kenkyū-buntansha) |
武知 正晃 広島大学, 医系科学研究科(歯), 准教授 (00304535)
重石 英生 広島大学, 医系科学研究科(歯), 講師 (90397943)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 核酸認識機構 / 口腔粘膜上皮細胞 / 抗菌ペプチド / 口腔粘膜炎症性疾患 / LL-37 / 口腔粘膜細胞 / 口腔粘膜上皮 / 抗菌ペプチドLL-37 |
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| Outline of Final Research Achievements |
The mechanism of nucleic acid recognition in oral mucosa is unknown. On the other hand, the antimicrobial peptide LL-37 is detected in epithelial inflammatory diseases. However, it is well unknown whether LL-37 is associated with inflammatory responses induced by nucleic acid, in oral mucosa. Therefore, we examined the effect of LL-37 on nucleic acid-mediated inflammatory responses in immortalized human oral keratinocytes (RT7). From those results, LL-37 dramatically increased self and non-self nucleotides-mediated CXCL10 expression in RT7, and those inductions were associated with NF-κB signaling activation. We found that LL-37 enables those nucleic acids to translocate into cytoplasm. In conclusion, LL-37 promotes exogenous nucleic acids-mediated inflammatory responses in oral keratinocytes, and that may be involved in the development of oral mucosal inflammatory diseases.
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| Academic Significance and Societal Importance of the Research Achievements |
今回の研究によって口腔粘膜細胞が, 自己DNAや非自己DNAと結合し，T細胞活性化因子などの炎症性遺伝子の発現誘導を行っていること，また唾液など工区に存在する抗菌ペプチドLL-37 がそれらの自己，非自己DNAを口腔粘膜上皮細胞内に導入し，核酸で誘導される免疫応答を調節している可能性を明らかにした。今回の研究成果は，口腔粘膜の新規免疫応答機構を解明するだけでなく，口腔粘膜炎症性疾患に対する新たな治療や，検査法への開発につながることが期待できると考えている。
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