Fetal inflammation is associated with persistent systemic and hippocampal inflammation and dysregulation of hippocampal glutamatergic homeostasis

Inflammation is a major cause of preterm birth and often

Hippocampal inflammation and dysregulation of glutamate metabolism persisted well into the postnatal period following i.a. LPS. Poor neurodevelopmental outcomes after FIRS in preterm infants may result in part through glutamatergically driven gray matter injury to the neonatal hippocampus.

Fetal rats were exposed to intra-amniotic (i.a.) LPS 2 days prior to birth to model FIRS. On postnatal day 7, expression of inflammatory mediators was measured in the liver, lung, and brain. Activation of microglia and expression of glutamatergic receptor subunits and transporters were measured in the hippocampus and cortex.

LPS caused persistent systemic inflammatory mediators gene expression. In the brain, there was corresponding activation of microglia in the hippocampus and cortex. Expression of inflammatory mediators persisted in the hippocampus, but not the cortex, and was associated with altered glutamatergic receptor subunits and transporters.