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.
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.
|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|