真核信号介导 GBS 毒力的双组分调节-猫眼课题宝

真核信号介导 GBS 毒力的双组分调节

批准号：

8663520

负责人：

Lakshmi Rajagopal

金额：

$48.24万

依托单位：

SEATTLE CHILDREN'S HOSPITAL

依托单位国家：

美国

项目类别：

财政年份：

2006

资助国家：

美国

项目状态：

已结题

起止时间：

2006-07-01 至 2014-12-31

来源：

https://reporter.nih.gov/project-details/8663520

关键词：

Amino Acids Amniotic Fluid Bacterial Infections Binding Biochemical Biological Biological Assay Blood - brain barrier anatomy Cavia Cells Cerebral Palsy Cesarean section Cytolysins DNA Binding Development Disease Epithelial Cells Evaluation Event Fetus Foundations Gene Expression Gene Expression Regulation Genes Genetic Genital system Genomics Goals Government Hemolysin Human Infection Inflammation Inflammatory Response Injury Invaded Lead Measures Mediating Membrane Mental Retardation Microbe Modeling Molecular Morbidity - disease rate Mus Neonatal Neonatal Mortality Neurologic Newborn Infant Organ Organism Pathogenesis Penetration Persons Phosphorylation Placenta Play Premature Birth Protein-Serine-Threonine Kinases Proteomics Public Health Regulation Repression Role Seizures Sepsis Signal Transduction Streptococcal Infections Streptococcus Group B System Testing Therapeutic Threonine Toxin Virulence Virulence Factors Woman antimicrobial peptide base defined contribution early onset fetal human NAT2 protein human mortality in utero insight intraamniotic infection mortality mutant neonatal morbidity novel pathogen perforin placental membrane prevent response sensor histidine kinase stillbirth transmission process

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中文摘要

翻译

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。B群链球菌（GBS）是人类新生儿早产、死产和早发性败血症的重要原因。虽然GBS通常以共生体形式存在于健康妇女的下生殖道（LGT）中，但促进GBS从LGT向胎儿传播的事件尚不清楚。宫内GBS感染上升的重要毒力因素尚未确定。利用人胎盘和豚鼠宫内感染模型，本研究的目的是确定激活毒力基因表达的分子机制，以促进GBS感染和胎儿损伤。

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. Virulence factors important for ascending in utero GBS infections have not been established. Using human placenta and a guinea pig model of intrauterine infection, the objective of this proposal is to define molecular mechanisms that activate virulence gene expression for ascending GBS infection and fetal injury.

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