| Project/Area Number |
26461652
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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 |
Embryonic/Neonatal medicine
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| Research Institution | Research Institute, Osaka Medical Center for Maternal and Child Health |
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Principal Investigator |
YANAGIHARA Itaru 地方独立行政法人大阪府立病院機構大阪府立母子保健総合医療センター(研究所), 免疫部門, 部長 (60314415)
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| Co-Investigator(Kenkyū-buntansha) |
北島 博之 地方独立行政法人大阪府立病院機構大阪府立母子保健総合医療センター(研究所), その他部局等, 新生児科主任部長 (10501041)
光田 信明 地方独立行政法人大阪府立病院機構大阪府立母子保健総合医療センター(研究所), その他部局等, 診療局長(兼産科主任部長) (50209805)
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| Research Collaborator |
MIMURA Kazuya
KAWAI Yasuhiro
NISHIUMI Fumiko
NAKAHIRA Kumiko
WU Heng Ning
NAKURA Yukiko
NAMBA Fumihiko
UCHIDA Kaoru
SAKA Ryuta
WAKIMOTO Tetsu
MEHANDJIEV R Tzvetozar
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | ウレアプラズマ / LPS / 水酸化フラーレン / チオレドキシン１ / 感染性流早産 / 早産 / 抗酸化 / 抗炎症 / 高感度細菌RNA同定 |
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| Outline of Final Research Achievements |
Intrauterine infection such as by Escherichia coli and Ureaplasma spp. induce placental inflammation and are one of the leading causes of preterm birth. We investigated the preventative effect of hydroxylated fullerene in a mouse preterm birth model induced by ureaplasmal TLR-2 ligand, UPM-1. The preterm birth rate decreased from 72.7% to 18.2% after an injection with hydroxylated fullerene in mice.
The preventative effect of thioredoxin-1 was also investigated in Escherichia coli lipopolysaccharide induced preterm birth mouse model. Recombinant human thoredoxin-1 prevented the rise of systemic proinflammatory cytokine levels in dam mice. After LPS challenge, placentas exhibited severe maternal vascular dilatation and congestion and a marked decidual neutrophil activation. These placental pathological findings were ameliorated by recombinant human thioredoxin-1, and the rate of inflammation-induced preterm delivery was attenuated.
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