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.

Public Health Relevance

Understanding environmental signals that regulate virulence gene expression and promote bacterial penetration of human placenta leading to fetal injury will be beneficial in therapeutic strategies against preterm birth, stillbirth and early onset neonatal infections.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Exploratory/Developmental Grants (R21)
Project #
1R21AI109222-01
Application #
8619390
Study Section
Special Emphasis Panel (ZRG1-IDM-B (80))
Program Officer
GU, Xin-Xing
Project Start
2013-12-01
Project End
2015-11-30
Budget Start
2013-12-01
Budget End
2014-11-30
Support Year
1
Fiscal Year
2014
Total Cost
$274,156
Indirect Cost
$133,563
Name
Seattle Children's Hospital
Department
Type
DUNS #
048682157
City
Seattle
State
WA
Country
United States
Zip Code
98105
Lannon, Sophia M R; Vanderhoeven, Jeroen P; Eschenbach, David A et al. (2014) Synergy and interactions among biological pathways leading to preterm premature rupture of membranes. Reprod Sci 21:1215-27