NEW MODEL OF ASCENDING INFECTION-RELATED PREMATURE BIRTH

感染相关早产上升的新模式

• 批准号: 7958877
• 负责人: CRAIG E. RUBENS
• 金额: $ 15.76万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-05-01 至 2010-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7958877
• 关键词: Biological Models; Brain Injuries; Cervical; Computer Retrieval of Information on Scientific Projects Database; Economics; Funding; Genital system; Grant; Human; Incidence; Infection; Inflammation; Inflammatory Response; Institution; Macaca nemestrina; Modeling; Molecular; Neonatal; Play; Premature Birth; Premature Labor; Preventive Intervention; Primates; Public Health; Research; Research Personnel; Resources; Role; Source; Streptococcus Group B; United States National Institutes of Health; Uterine Contraction; intraamniotic infection; nonhuman primate; premature

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Preterm birth remains a significant economic and public health burden and the incidence is rising. Infection induced inflammation plays a significant role in preterm birth and is thought to occur as a result of infection, which promotes premature uterine contractions. Obstetrical research has yet to identify effective preventive interventions for preterm labor. The overall objective of this proposal is to develop a model system which emulates human preterm birth to ultimately elucidate molecular mechanisms of infection-induced preterm labor and related adverse neonatal sequelae (e.g. brain injury). We propose to develop a nonhuman primate model in the pigtail macaque that closely mimics an ascending lower genital tract infection at the chorio-decidual interface in the lower uterine segment-decidual interface. The central hypothesis is that infection with group B streptococcus (GBS) at the chorio-decidual interface at the proximal cervical canal will result in an inflammatory response that results in premature myometrial contractions, intra-amniotic infection, and premature delivery.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 早产仍然是一个重大的经济和公共卫生负担，发病率正在上升。感染引起的炎症在早产中起着重要作用，并且被认为是由于感染而发生的，这促进了子宫过早收缩。产科研究尚未确定有效的预防早产的干预措施。本提案的总体目标是开发一个模拟人类早产的模型系统，以最终阐明感染诱导的早产和相关不良新生儿后遗症（例如脑损伤）的分子机制。我们打算培育一种非人类的灵长类动物 猪尾猕猴模型，在子宫下段-蜕膜界面中的绒毛膜-蜕膜界面处密切模仿上行性下生殖道感染。中心假设是近端宫颈管绒毛膜-蜕膜界面处的B组链球菌（GBS）感染将导致炎症反应，从而导致子宫肌层过早收缩、羊膜内感染和早产。