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.

Public Health Relevance

Understanding molecular mechanisms that mediate GBS penetration of placenta and fetal organs will be beneficial in therapeutic strategies against infections that lead to fetal injury, preterm births, stillbirths and early onset neonatal infectins.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
High Priority, Short Term Project Award (R56)
Project #
2R56AI070749-06A1
Application #
8663520
Study Section
Bacterial Pathogenesis Study Section (BACP)
Program Officer
GU, Xin-Xing
Project Start
2006-07-01
Project End
2014-05-31
Budget Start
2013-06-11
Budget End
2014-05-31
Support Year
6
Fiscal Year
2013
Total Cost
$482,356
Indirect Cost
$234,994
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