Galectin-3 inhibition prevents preterm birth induced by dental infection of Porphyromonas gingivalis.

2015 Fiscal Year Final Research Report

• 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
• 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

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.

Free Research Field

口腔病理学