LPS alters placental inflammatory and endocrine mediators and inhibits fetal neurite growth in affected offspring during late gestation

Introduction During pregnancy, maternal infection at different stages of gestation increases the risk of developing several psychiatric and neurological disorders later in life for affected offspring. As placental health is intrinsically linked to neurodevelopmental outcome, maternal infection may adversely affect the placenta at or before the gestational stages it affects fetal neurodevelopment. Here we examined this premise. Methods Pregnant-Sprague Dawley rats were administered saline or lipopolysaccharide by intraperitoneal injection on embryonic days 12-18. We then examined a number of key placental inflammatory and endocrine mediators, along with fetal, birth and neuronal characteristics at different stages of development. Results Maternal exposure to lipopolysaccharide at later gestational ages significantly increased pro-inflammatory IL-1β expression and reduced placental HSD11B2 expression. This was accompanied by a reduction in placental weight and embryo number without an effect on embryo weight or crown-rump length. In utero lipopolysaccharide exposure at later gestational ages also impaired the growth of neurons from affected offspring. Discussion These data show that maternal infection at later gestational ages modifies placental inflammatory and endocrine mediators that may adversely affect the growth of developing neurons in affected offspring.