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UREAPLASMA INVASION OF CHORION AND AMNION EPITHELIAL CELL LAYERS IN VITRO

UREAPLASMA INVASION OF CHORION AND AMNION EPITHELIAL CELL LAYERS IN VITRO
体外解脲支原体对绒毛膜和羊膜上皮细胞层的侵袭
批准号:
8357846
负责人:
Peta Louise Grigsby
金额:
$1.82万
依托单位国家:
美国
项目类别:
财政年份:
2011
资助国家:
美国
项目状态:
已结题
起止时间:
2011-05-01 至 2012-04-30

项目摘要

项目成果

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中文摘要
翻译
这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的, 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量, 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 在上行感染期间,绒毛膜蜕膜是接触病原体的第一线屏障,病原体可以穿过膜并感染羊膜和羊水。毒性细菌如B组链球菌或E.大肠杆菌在体外已经显示出粘附、侵入和转胞吞穿过完整的绒毛膜羊膜。然而,体内局部炎症反应可能会削弱绒毛膜羊膜的结构完整性,并允许毒性较低的微生物也突破这一屏障。例如,据报道,粘膜表面病原体如人型支原体或脲原体在妊娠早期感染羊膜腔,而不会导致胎膜破裂。尽管如此,没有直接的实验证据证明美国的。小虫可以破坏完整的绒毛膜羊膜并进入羊膜腔。这一系列体外研究将扩展和补充从我们的实验性绒毛膜蜕膜模型获得的体内数据。U.将在一系列实验条件(绒毛膜蜕膜暴露与羊膜暴露)下测定小孢子。组成组织层的特异性生物标志物的差异产生率将阐明子宫内感染(绒毛膜蜕膜vs.羊膜内感染)期间在羊水和宫颈阴道液(CVF)中观察到的特异性生物标志物谱的组织来源。此外,这些研究将提供重要的信息,羊膜或绒毛膜蜕膜的贡献,炎症反应后,U。子宫内暴露。
英文摘要
This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. During ascending infection, the choriodecidua is the first-line barrier in contact with pathogens that can cross the membranes and infect the amnion and amniotic fluid. Virulent bacteria such as group B Streptococci or E. coli have been shown in vitro to adhere, invade and transcytose through intact chorioamniotic membranes. However, localized inflammatory response in vivo is likely to weaken the structural integrity of the chorioamnion and to allow a less virulent microorganism to also breech this barrier. For instance, mucosal surface pathogens such as Mycoplasma hominis or Ureaplasma species have been reported to infect the amniotic cavity quite early in gestation without rupture of the fetal membranes. Despite this, there is no direct experimental evidence demonstrating that U. parvum can breech the intact chorioamniotic membranes and gain entry into the amniotic cavity. This series of in vitro studies will extend and complement the in vivo data obtained from our experimental choriodecidual model. Transmigration of U. parvum will be determined under a series of experimental conditions (choriodecidual exposure vs. amniotic exposure). Differential production rates of specific biomarkers by component tissue layers will illuminate the tissue source of specific biomarker profiles observed in the amniotic fluid and cervical vaginal fluid (CVF) during intra-uterine infection (choriodecidual vs. intra-amniotic infection). Moreover, these studies will provide important information on the contribution of the amnion or choriodecidua to the inflammatory response following U. parvum exposure in utero.
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Primate model of mid-gestation Ureaplasma in utero infection: Prevention of neuro
Primate model of mid-gestation Ureaplasma in utero infection: Prevention of neuro
Primate model of mid-gestation Ureaplasma in utero infection: Prevention of neuro
Primate model of mid-gestation Ureaplasma in utero infection: Prevention of neuro
国内基金
海外基金
Segmented Filamentous Bacteria激活宿主免疫系统抑制其拮抗菌 Enterobacteriaceae维持菌群平衡及其机制研究
  • 批准号:
    81971557
  • 项目类别:
    面上项目
  • 资助金额:
    65.0万元
  • 批准年份:
    2019
  • 负责人:
    毛开睿
  • 依托单位:
电缆细菌(Cable bacteria)对水体沉积物有机污染的响应与调控机制