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.
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.
