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: OREGON HEALTH & SCIENCE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-05-01 至 2012-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8357846
• 关键词: Amniotic Fluid; Bacteria; Biological Markers; Cervical; Chorion; Complement; Data; Epithelial Cells; Escherichia coli; Fetal Membranes; Funding; Grant; In Vitro; Infection; Inflammatory Response; Invaded; Membrane; Modeling; Mycoplasma hominis; National Center for Research Resources; Perinatal Exposure; Pregnancy; Primates; Principal Investigator; Production; Reporting; Research; Research Infrastructure; Resources; Rupture; Series; Source; Streptococcus Group B; Surface; Tissues; United States National Institutes of Health; Ureaplasma; Virulent; amnion; amniotic cavity; cost; in vivo; intraamniotic infection; microorganism; pathogen; vaginal fluid

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.

该子项目是利用资源的众多研究子项目之一 由 NIH/NCRR 资助的中心拨款提供。子项目的主要支持 并且子项目的主要研究者可能是由其他来源提供的， 包括其他 NIH 来源。 子项目可能列出的总成本 代表子项目使用的中心基础设施的估计数量， NCRR 赠款不直接向子项目或子项目工作人员提供资金。 在上行感染过程中，绒毛膜蜕膜是与病原体接触的第一道屏障，病原体可以穿过膜并感染羊膜和羊水。 B 族链球菌或大肠杆菌等强毒细菌在体外已被证明可以通过完整的绒毛膜羊膜粘附、侵入和转胞吞。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突破这一屏障。例如，据报道，诸如人型支原体或解脲支原体等粘膜表面病原体可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表明微小 U. parvum 可以破坏完整的绒毛膜羊膜并进入羊膜腔。这一系列的体外研究将扩展和补充从我们的实验性脉络膜蜕膜模型获得的体内数据。小 U. parvum 的迁移将在一系列实验条件下确定（绒毛膜蜕膜暴露与羊膜暴露）。各组成组织层的特定生物标志物的差异产生率将阐明在子宫内感染（绒毛膜蜕膜与羊膜内感染）期间在羊水和宫颈阴道液（CVF）中观察到的特定生物标志物谱的组织来源。此外，这些研究将提供有关羊膜或绒毛膜蜕膜对子宫内接触小 U. parvum 后炎症反应的重要信息。