调节 GBS 毒力的环境信号-猫眼课题宝

调节 GBS 毒力的环境信号

批准号：

8619390

负责人：

Lakshmi Rajagopal

金额：

$30.46万

依托单位：

SEATTLE CHILDREN'S HOSPITAL

依托单位国家：

美国

项目类别：

财政年份：

2013

资助国家：

美国

项目状态：

已结题

起止时间：

2013-12-01 至 2015-11-30

来源：

https://reporter.nih.gov/project-details/8619390

关键词：

Acidity Amniotic Fluid Bacteria Bacterial Infections Biological Blood - brain barrier anatomy Cavia Cells Cerebral Palsy Cesarean section DNA Binding Development Epithelial Cells Epithelium Event Fetus Foundations Gene Expression Genes Genital system Goals Human Infection Inflammation Inflammatory Response Injury Invaded Measures Membrane Mental Retardation Microbe Modeling Morbidity - disease rate Mus Neonatal Neonatal Mortality Neurologic Newborn Infant Pathogenesis Penetration Perinatal Phosphorylation Placenta Play Pregnancy Premature Birth Protein-Serine-Threonine Kinases Public Health Regulation Repression Role Seizures Sepsis Signal Transduction Streptococcal Infections Streptococcus Group B Structure System Testing Therapeutic Threonine Uterus Vagina Virulence Virulence Factors Woman antimicrobial peptide base early onset fetal fetal infection human mortality in utero insight intraamniotic infection microorganism mortality neonatal morbidity neonate novel pathogen placental membrane pregnant prevent public health relevance response sensor histidine kinase stillbirth transmission process

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中文摘要

翻译

描述（由申请方提供）：人类新生儿的发病率和死亡率是重大的公共卫生问题。B族链球菌（GBS）是人类新生儿中早产、死胎和早发性脓毒症的重要原因。虽然GBS通常以尿道形式存在于健康女性的下生殖道（LGT）中，但促进GBS从LGT传播至胎儿的事件尚不清楚。使用人胎盘和豚鼠模型的宫内感染，本建议的目的是定义环境信号，激活上行GBS感染和胎儿损伤的毒力基因表达。

英文摘要

DESCRIPTION (provided by applicant): Morbidity and mortality of human newborns are significant public health concerns. Group B Streptococci (GBS) are a significant cause of preterm births, stillbirths and early onset sepsis in human newborns. Although GBS normally reside as commensals in the lower genital tract (LGT) of healthy women, the events that promote transmission of GBS from the LGT to the fetus are unknown. Using human placenta and a guinea pig model of intrauterine infection, the objective of this proposal is to define environmental signals that activate virulence gene expression for ascending GBS infection and fetal injury.

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