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A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
Male fetus susceptibility to maternal inflammation: C-reactive protein and brain development
Sharon K Hunter1, M Camille Hoffman1,2, Angelo D'Alessandro3
1Departments of Psychiatry, University of Colorado Denver School of Medicine, Aurora, Colorado80045, USA.
Insights
Maternal inflammation during pregnancy affects fetal brain development, particularly in males, impacting cerebral inhibition. Early interventions like prenatal choline may mitigate risks for later mental illness.
Area of Science:
- Neuroscience
- Developmental Psychology
- Prenatal Medicine
Background:
- Maternal inflammation in early pregnancy is a risk factor for offspring mental illness.
- Early newborn manifestations of maternal inflammation's effects on fetal brain development are poorly understood.
Purpose of the Study:
- To investigate the effects of maternal inflammation on newborn cerebral inhibition and infant behavior.
- To explore sex-dependent differences in these effects.
- To assess the role of maternal choline levels.
Main Methods:
- Assessed maternal inflammation markers (CRP, cytokines, choline) at 16 weeks gestation.
- Measured infant cerebral inhibition (P50 sensory gating) at 1 month.
- Evaluated infant behavior via maternal ratings at 3 months.
Main Results:
- Maternal CRP reduced cerebral inhibition in male newborns but increased it in females.
- Sex-dependent effects were observed in infant self-regulatory behaviors.
- Higher maternal choline levels partially counteracted CRP's effects in males.
Conclusions:
- The male fetal-placental unit is more vulnerable to maternal inflammation, impacting cerebral inhibition.
- Early deficits in cerebral inhibition may predict later mental illness, such as schizophrenia.
- Prenatal interventions, including choline, may prevent long-term mental health consequences.
Background:
Maternal inflammation in early pregnancy has been identified epidemiologically as a prenatal pathogenic factor for the offspring's later mental illness. Early newborn manifestations of the effects of maternal inflammation on human fetal brain development are largely unknown.
Methods:
Maternal infection, depression, obesity, and other factors associated with inflammation were assessed at 16 weeks gestation, along with maternal C-reactive protein (CRP), cytokines, and serum choline. Cerebral inhibition was assessed by inhibitory P50 sensory gating at 1 month of age, and infant behavior was assessed by maternal ratings at 3 months of age.
Results:
Maternal CRP diminished the development of cerebral inhibition in newborn males but paradoxically increased inhibition in females. Similar sex-dependent effects were seen in mothers' assessment of their infant's self-regulatory behaviors at 3 months of age. Higher maternal choline levels partly mitigated the effect of CRP in male offspring.
Conclusions:
The male fetal-placental unit appears to be more sensitive to maternal inflammation than females. Effects are particularly marked on cerebral inhibition. Deficits in cerebral inhibition 1 month after birth, similar to those observed in several mental illnesses, including schizophrenia, indicate fetal developmental pathways that may lead to later mental illness. Deficits in early infant behavior follow. Early intervention before birth, including prenatal vitamins, folate, and choline supplements, may help prevent fetal development of pathophysiological deficits that can have life-long consequences for mental health.
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