Global Alliance to Prevent Prematurity and Stillbirth: Specimen Respository Network
David A Eschenbach, MD, Principal Investigator
The Washington State Prematurity Research Network (WSPRN) is a new and innovative statewide network that collects prospective data and specimens from a cohort of pregnant women to promote the discovery of preterm birth causes and interventions. This coalition of hospitals, providers, and researchers focuses on preventing preterm birth by facilitating new research and improving the quality of prenatal care. Specimens and data will be processed and stored at the GAPPS Repository, which is part of the Seattle Children's Research Institute (SCRI). This critical research resource will allow investigators to answer a broad range of scientific questions about maternal, fetal and newborn health. This effort is led by the Global Alliance to Prevent Prematurity and Stillbirth (GAPPS), an initiative of Seattle Children's that is leading a collaborative, global effort to increase awareness and accelerate innovative research and interventions to improve maternal, newborn and child health outcomes.
Funding Source: Seattle Children's Hospital Research Institute/Gates Foundation
End Date: 12-31-16
GBS-Mediated In Utero Fetal Injury
Kristina M Adams Waldorf, MD, Co-Principal Investigator with Lakshmi Rajagopal, PhD
Morbidity and mortality of human newborns are significant public health concerns. Predominant risk factors for neonatal morbidity and mortality are invasive bacterial infections and the ensuing severe inflammatory response, which mainly begin in utero. Group B Streptococci (GBS) are a significant cause of preterm births, stillbirths and early onset neonatal disease. Factors that facilitate ascending GBS infection from the lower genital tract to the fetus are not understood. Our studies indicate that upregulation of virulence factors facilitate GBS invasion of placental membranes, in vitro. Using human placental membranes and a nonhuman primate model, the objective of this proposal is to mechanistically define how virulence factors enable ascending in utero GBS infection and subsequent fetal lung and brain injury.
Funding Source: National Institutes of Health/ (NIH/NIAID)
End Date: 6-30-17
Environmental Signals that Regulate GBS Virulence
Kristina M Adams Waldorf, MD, Co-Investigator, with Lakshmi Rajagopal, PhD, Principal Investigator
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.
Funding Source: National Institutes of Health (NIH/NIAID)
End Date: 11-30-15
Targeting Leukocyte Activation to Prevent Preterm Labor
Kristina M Adams Waldorf, MD, Co-Investigator, with Stephen Lye, PhD, Principal Investigator (University of Toronto)
The objectives of this proposal are 1) to determine whether peripheral leukocyte activation is associated with labor, 2) analyze how cytokines produced by laboring myometrium activate leukocytes, and 3) use a unique, chronically catheterized, nonhuman primate model of preterm labor to determine whether blockade of this peripheral leukocyte activation and the consequent uterine inflammation through administration of a broad spectrum chemokine inhibitor can prevent infection-induced preterm labor.
Funding Source: Burroughs-Wellcome Fund
End Date: 5-30-18