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Fetal sepsis in utero induces disruption of gene networks involved in cardiac morphogenesis in a nonhuman primate model of infection-induced preterm labor

ABSTRACT: Fetal lung and brain injury have been linked with intrauterine exposure to amniotic fluid (AF) cytokines, but injury to other fetal organs are not well characterized. Fetal cardiac injury was suspected based on an ultrasound study suggesting diastolic dysfunction, but not previously confirmed or characterized. In this study we explore the relationship between cytokine exposure due to exposure to group B streptococcus and cardiac gene expression.

ORGANISM(S): Macaca nemestrina Macaca fascicularis Macaca mulatta

PROVIDER: GSE98459 | GEO | 2018/01/23

REPOSITORIES: GEO

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A bacterial hemolytic lipid toxin subverts neutrophils and neutrophil extracellular traps to promote gbs invasion, fetal injury and preterm labor in nonhuman primates

Project description:Preterm birth is a leading cause of neonatal morbidity and mortality. Microbial infection and inflammation of the amniotic cavity are associated with the majority of early preterm births and thought to arise from ascension of bacteria from the lower genital tract. Group B Streptococci (GBS) are beta-hemolytic, gram-positive bacteria, which commonly colonize the vagina and have been recovered from the amniotic fluid in cases of preterm birth. Host immune defenses that are critical for prevention of microbial invasion of the amniotic cavity (MIAC) and preterm labor are not completely understood. We recently showed that increased expression of the hemolytic pigment promotes GBS penetration of human placenta ex vivo and hyperhemolytic/hyperpigmented GBS strains with mutations in the hemolysin repressor (CovR/CovS) can be isolated from women in preterm labor. To understand placental/ choriodecidual immune responses that are necessary to prevent MIAC and preterm labor, we utilized a unique chronically catheterized nonhuman primate model that closely emulates human pregnancy. We observed that preterm labor, MIAC, and fetal injury occurred significantly more frequently in pregnant nonhuman primates infected with hyperpigmented GBS (ΔcovR) despite the strong induction of proinflammatory responses in the chorioamnion. Placental histopathology revealed a systematic progression in development of chorioamnionitis in GBSΔcovR animals beginning with chorionic vasculitis and subsequently progressing to neutrophilic infiltration in the chorioamnion.

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Choriodecidual Infection Downregulates Angiogenesis and Morphogenesis Pathways in Fetal Lungs from Macaca Nemestrina

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