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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Role of the fetus in perinatal infection and neonatal brain damage
1Department of Neurology, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Insights
Perinatal infection increases infant brain injury risk. The fetal inflammatory response, indicated by elevated cytokines and inflammatory cells, is a key contributor to neonatal brain injury and developmental issues.
Area of Science:
- Neonatal neurology
- Immunology
- Developmental pediatrics
Background:
- Perinatal infection is increasingly linked to adverse infant outcomes.
- The fetal inflammatory response is a critical factor in neonatal brain injury.
Purpose of the Study:
- To explore the role of the fetal inflammatory response in neonatal brain injury.
- To examine the evidence linking perinatal infection to developmental disabilities.
Main Methods:
- Review of evidence on fetal inflammatory response markers (cytokines, inflammatory cells).
- Analysis of the contribution of fetal inflammation to neonatal brain injury and developmental outcomes.
Main Results:
- Elevated cytokines in amniotic fluid/fetal circulation indicate humoral inflammatory response.
- Inflammatory cells in placental/umbilical cord tissues show morphologic inflammatory response.
- Fetal inflammatory response is a significant factor in neonatal brain injury and developmental disability.
Conclusions:
- The fetal inflammatory response, not maternal factors, is implicated in neonatal brain injury.
- Interventions should prioritize fetal protection against inflammatory insults.
Abstract:
Increasing evidence supports the view that infants exposed to perinatal infection are at increased risk for brain injury. We suggest that elevated cytokines in the amniotic fluid or in the fetal circulation be viewed as a humoral expression and that inflammatory cells in chorionic plate or umbilical cord blood vessel walls be viewed as a morphologic expression of the fetal inflammatory response. We discuss the evidence supporting the hypothesis that the fetal inflammatory response contributes to neonatal brain injury and later developmental disability. Little support has been found for a maternal contribution. Intervention should be designed with the fetus in mind.
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