Prenatal exposure to maternal infection alters cytokine expression in the placenta, amniotic fluid, and fetal brain

@article{Urakubo2001PrenatalET,
  title={Prenatal exposure to maternal infection alters cytokine expression in the placenta, amniotic fluid, and fetal brain},
  author={Ari Urakubo and L. Fredrik Jarskog and Jeffrey A. Lieberman and John H. Gilmore},
  journal={Schizophrenia Research},
  year={2001},
  volume={47},
  pages={27-36}
}
The role of cytokines in mediating effects of prenatal infection on the fetus: implications for schizophrenia
TLDR
Data suggest that effects of maternal LPS exposure on the developing fetal brain are not mediated by the direct action of LPS, but via indirect actions at the level of the maternal circulation or placenta.
Maternal LPS induces cytokines in the amniotic fluid and corticotropin releasing hormone in the fetal rat brain.
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The findings suggest that maternal infections may lead to an unbalanced inflammatory reaction in the fetal environment that activates the fetal stress axis.
LPS Exposure Increases Maternal Corticosterone Levels, Causes Placental Injury and Increases IL-1Β Levels in Adult Rat Offspring: Relevance to Autism
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Pregnant Wistar rats exposed to lipopolysaccharide induced autistic-like behavioral and immune disturbances in childhood and adulthood, indicating that this model is a robust rat model of autism.
Maternal immune activation alters the behavioral, cytokine, and gene expression profiles in rat offspring
TLDR
The following dissertation addressed the behavioral, immunological, and molecular effects of MIA in the offspring of pregnant Sprague-Dawley rats given an intraperitoneal injection of lipopolysaccharide (LPS) on embryonic day 15.
Interleukin-6 in the Maternal Circulation Reaches the Rat Fetus in Mid-gestation
TLDR
The permeability of the rat placental barrier to IL-6 is much higher in mid-gestation than in late pregnancy, suggesting that maternally derived IL- 6 may directly induce fetal injury but also stimulate the release of fetal stress hormones which might lead to disease at adult age.
Prenatal Exposure to Lipopolysaccharide Alters Renal DNA Methyltransferase Expression in Rat Offspring
TLDR
The findings suggest that prenatal exposure to LPS may result in changes of intrarenal DNMTs through the IL-6/Fli-1 pathway and TNF-α, which probably involves hypertension in offspring due to maternal exposure to inflammation.
Effects of Perinatal Lipopolysaccharide (LPS) Exposure on the Developing Rat Brain; Modeling the Effect of Maternal Infection on the Developing Human CNS
TLDR
The data demonstrate that perinatal LPS exposure impacts the developing cerebellum in strain- and sex-dependent manner via complex mechanisms that involve changes in oxidative stress, enzymes involved in maintaining local TH homeostasis, and downstream gene expression.
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References

SHOWING 1-10 OF 75 REFERENCES
Maternal Intrauterine Infection, Cytokines, and Brain Damage in the Preterm Newborn
TLDR
Unifying models postulate how proinflammatory cytokines might lead to IVH and neonatal white matter damage during prenatal maternal infection and intervene to prevent later disability in those born near the end of the second trimester.
Fetal but not maternal serum cytokine levels correlate with histologic acute placental inflammation.
TLDR
It is concluded that fetal serum, but not maternal serum cytokine levels, are correlated with histologic evidence of acute placental inflammation, and may reflect a predominant placental origin of the cytokines.
Induction of cytokine transcripts in the central nervous system and pituitary following peripheral administration of endotoxin to mice
TLDR
The capacity of brain cells to synthesize different cytokine mRNAs in vivo is shown and the kinetics of their expression in several brain areas and in the periphery in parallel to the activation of a neuroendocrine pathway by endotoxin is defined.
Exposure to Acute Stress Induces Brain Interleukin-1β Protein in the Rat
TLDR
Elimination of the stress-induced rise in corticosterone unmasked a robust and widespread increase in brain IL-1β, possibly suppressed by the rapid and prolonged high levels of glucocorticoids produced by IS.
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