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

ABSTRACT:

Background

Inflammation is a major cause of preterm birth and often results in a fetal inflammatory response syndrome (FIRS). Preterm infants with FIRS have a higher childhood incidence of neurodevelopmental disability than preterm infants without FIRS. The mechanisms connecting FIRS to neurodevelopmental disability in formerly preterm infants are not fully understood, but the effect on premature gray matter may have an important role.

Methods

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.

Results

SUBMITTER: Gisslen T 

PROVIDER: S-EPMC6435426 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature