Project/Area Number |
26670802
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
Morphological basic dentistry
|
Research Institution | Hiroshima University |
Principal Investigator |
Takata Takashi 広島大学, 医歯薬保健学研究院(歯), 教授 (10154783)
|
Co-Investigator(Kenkyū-buntansha) |
Miyauchi Mutsumi 広島大学, 医歯薬保健学研究院(歯), 准教授 (50169265)
Kitagawa Masae 広島大学, 病院, 助教 (10403627)
Furusho Hisako 広島大学, 医歯薬保健学研究院(歯), 助教 (00634461)
|
Project Period (FY) |
2014-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 早産 / 歯性感染 / Porphyromonas gingivalis / Galectin-3 / N-アセチルラクトサミン / TNF-a / COX-2 / 早期低体重児出産 / 胎盤栄養細胞 / LPS |
Outline of Final Research Achievements |
Epidemiological studies have revealed a link between dental infection and preterm birth (PB), however, the underlying mechanisms remain unclear. Previously we showed galectin-3 upregulated in Pg infected placenta. In the present study, we examined the effects of N-acetyllactosamine (NLac: an inhibitor of Gal-3)on Pg-dental infection induced PB. The injection of NLac (20gd) significantly prevented PB induced by Pg infection (17.7gd). Pg-dental infection induced TNF-a and COX-2 upregulation was reduced in NLac-Pg. NLac suppressed the expression of TNF-a, COX-2 and Galectin-3 by Pg-LPS from torophoblasts in dose dependent manner. NLac suppresses inflammatory mediators, which promote delivery, by inhibiting the effect of Galectin-3 and prevents PB induced by Pg-dental infection. Therefore, NLac may be a novel preventive/therapeutic strategy for PB.
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