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

项目摘要

项目成果

Lakshmi Rajagopal的其他基金

相似基金

相关文献

中文摘要

翻译

点击翻译按钮获取中文摘要

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.

期刊论文(0)

专著(0)

科研奖励(0)

会议论文