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Cited by 405Tryptophan and brain disordersPreterm Birth and ChorioamnionitisNeuroinflammation and Neurodegeneration Mechanisms

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

Urakubo, Ari, Jarskog, L.Fredrik, Lieberman, Jeffrey A., Gilmore, John H.·2001·Schizophrenia Research
DOI 10.1016/s0920-9964(00)00032-3
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Abstract

Prenatal exposure to infection appears to increase the risk of schizophrenia and other neurodevelopmental disorders. We have hypothesized that cytokines, generated in response to maternal infection, play a key mechanistic role in this association. E16 timed pregnancy rats were injected i.p. with Escherichia coli lipopolysaccharide (LPS) to model prenatal exposure to infection. Placenta, amniotic fluid and fetal brains were collected 2 and 8h after LPS exposure. There was a significant treatment effect of low-dose (0.5mg/kg) LPS on placenta cytokine levels, with significant increases of interleukin (IL)-1beta (P<0.0001), IL-6 (P<0.0001), and tumor necrosis factor-alpha (TNF-alpha) (P=0.0001) over the 2 and 8h time course. In amniotic fluid, there was a significant effect of treatment on IL-6 levels (P=0.0006). Two hours after maternal administration of high-dose (2.5mg/kg) LPS, there were significant elevations of placenta IL-6 (P<0.0001), TNF-alpha (P<0.0001), a significant increase of TNF-alpha in amniotic fluid (P=0.008), and a small but significant decrease in TNF-alpha (P=0.035) in fetal brain. Maternal exposure to infection alters pro-inflammatory cytokine levels in the fetal environment, which may have a significant impact on the developing brain.

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  • In the common MIA model, challenging pregnant rodents with infection or poly(I:C) causes significant immunological, neurodevelopmental, and behavioral changes in the offspring.

    “The MIA model in its most common design involves challenging pregnant rodents via direct infection (eg, influenza, Escherichia coli) or the dsRNA mimic poly (I:C); significant immunological, neurodevelopmental, and behavioral changes are then observed in the offspring”

    From The Role of the Immune System in Autism Spectrum Disorder (2017) · cites this paper as Urakubo et al, 2001

  • The maternal immune activation model has repeatedly produced consistent results and supports a subset of autism with autism-relevant atypical behaviors.

    “Some of the strongest support for maternal infection as a contributor to autism has come from the maternal immune activation (MIA) model, which has repeatedly shown consistent results, helping to establish a subset of autism that is supported by observations of autism-relevant atypical behaviors.”

    From The Role of the Immune System in Autism Spectrum Disorder (2017) · cites this paper as Urakubo et al, 2001

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Authors
Urakubo, A., Jarskog, L. F., Lieberman, J. A., & Gilmore, J. H.
Affiliations
University of North Carolina at Chapel Hill (US)
Corresponding author
Gilmore, John H.
ORCID
Venue
Schizophrenia Research
Publisher
Elsevier BV
Published
2001-01
Volume
47
Issue
1
Pages
27-36
ISSN
0920-9964 (ISSN-L)
DOI
10.1016/s0920-9964(00)00032-3
OpenAlex
W2013263136
Cited by
405
References
78
Citations by year
2026: 5 · 2025: 7 · 2024: 10 · 2023: 16 · 2022: 15 · 2021: 19 · 2020: 20 · 2019: 20 · 2018: 24 · 2017: 12 · 2016: 20 · 2015: 19 · 2014: 17 · 2013: 25 · 2012: 20
FWCI
3.94
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Schizophrenia Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Mental Health (MH 33127)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Health Sciences › Medicine › Epidemiology › Preterm Birth and Chorioamnionitis
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
prenatal infection, maternal infection
MeSH terms
Amniotic Fluid, Animals, Brain, Escherichia coli, Female, Fetus, Lipopolysaccharides, Maternal-Fetal Exchange, Placenta, Pregnancy, Pregnancy Complications, Infectious, Prenatal Exposure Delayed Effects, Cytokines, Rats, Sprague-Dawley, Rats

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