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

Research Project

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
Project Status	Completed (Fiscal Year 2014)
Budget Amount *help	¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000) Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000) Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000) Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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 / 妊娠ヒツジ / ポリミキシン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.