The research on how intrauterine inflammation transmit to fetus by the intermediary of fetal skin with using ovine model.

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592458
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Obstetrics and gynecology
• Research Institution: Tohoku University
• Principal Investigator: SAITO Masatoshi 東北大学, 大学病院, 助教 (00451584)
• Co-Investigator(Kenkyū-buntansha): MATSUDA Tadashi 東北大学, 大学病院, 准教授 (50361100) ; SUGAWARA Junichi 東北大学, 東北メディカル・メガバンク機構, 教授 (60280880)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 早産 / 子宮内感染 / 子宮内炎症 / 胎児皮膚組織 / 炎症性サイトカイン / Polymyxin B

Outline of Final Research Achievements

Intrauterine infection is a leading cause of preterm birth, most notably in deliveries occurring before 32 weeks gestation. However, the details of the mechanism and pathway from intrauterine infection to fetal inflammation are still unknown. We made an intrauterine inflammation model with using pregnant sheep, and also could indicate that a cationic peptide antibiotic, Polymyxin B have a possibility to calm the intrauterine inflammation down causing with Escherichia coli lipopolysaccharides (LPS) in fetal skin tissue with decreasing of the expression of messenger RNA of inflammatory cytokines such as IL-1 beta, TNF-alpha, IL-6, IL-8 and MCP-2.
These data are consistent with a partial resolution of LPS-driven intrauterine inflammation. They suggest the potential for agonist capture as a conceptual means of resolving the pro-parturition inflammation caused by infection of the amniotic cavity.

Free Research Field

周産期医学　胎児生理学