GBS mediated in utero fetal injury

GBS介导的子宫胎儿损伤

基本信息

批准号：
8688141
负责人：
KRISTINA M. ADAMS WALDORF
金额：
$ 77.16万
依托单位：
SEATTLE CHILDREN'S HOSPITAL
依托单位国家：
美国
项目类别：
财政年份：
2012
资助国家：
美国
起止时间：
2012-07-01 至 2017-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8688141
关键词：
Amniotic Fluid Animal Model Animals Antibiotic Prophylaxis Bacteria Bacterial Infections Brain Injuries Cells Cytolysins Development Disease Epithelium Escherichia coli Evaluation Exposure to Fetal Lung Fetal Membranes Fetus Foundations Gardnerella Gene Expression Regulation Genital system Government Hemolysin Human Immunomodulators In Vitro Infection Inflammation Inflammatory Response Injury Invaded Knowledge Lead Link Listeria Measures Mediating Mediator of activation protein Membrane Membrane Protein Traffic Modeling Morbidity - disease rate Mothers Nature Neonatal Neonatal Mortality Newborn Infant Organism Pathogenesis Perinatal Persons Pregnancy Premature Birth Public Health Resolution Risk Risk Factors Role Sampling Signal Pathway Signal Transduction Simulate Streptococcal Infections Streptococcus Group B System Toll-like receptors Toxin Up-Regulation Vaccines Virulence Virulence Factors Woman amniotic cavity early onset fetal fetal infection human mortality immune activation in utero inhibitor/antagonist intrapartum lung injury mutant neonatal morbidity nonhuman primate novel novel therapeutics pathogen perforin placental membrane stillbirth therapeutic development trafficking transmission process

项目摘要

DESCRIPTION (provided by applicant): Morbidity and mortality of human newborns are significant public health concerns. Predominant risk factors for neonatal morbidity and mortality are invasive bacterial infections and the ensuing severe inflammatory response, which mainly begin in utero. Group B Streptococci (GBS) are a significant cause of preterm births, stillbirths and early onset neonatal disease. Factors that facilitate ascending GBS infection from the lower genital tract to the fetus are not understood. Our studies indicate that upregulation of virulence factors facilitate GBS invasion of placental membranes in vitro. Using human placental membranes and a nonhuman primate model, the objective of this proposal is to mechanistically define how virulence factors enable ascending in utero GBS infection and subsequent fetal lung and brain injury.

描述（由申请人提供）：人类新生儿的发病率和死亡率是重大的公共卫生问题。新生儿发病和死亡的主要危险因素是侵袭性细菌感染和随之而来的严重炎症反应，这些反应主要始于子宫内。 B 族链球菌 (GBS) 是早产、死产和早发新生儿疾病的重要原因。促进 GBS 感染从下生殖道上升到胎儿的因素尚不清楚。我们的研究表明，毒力因子的上调有利于 GBS 体外侵入胎盘膜。该提案的目的是使用人类胎盘膜和非人类灵长类动物模型，从机械上定义毒力因子如何导致子宫内 GBS 感染上升以及随后的胎儿肺和脑损伤。