Cited by 177Tryptophan and brain disordersNeuroinflammation and Neurodegeneration MechanismsNeonatal and fetal brain pathology

Maternal poly I:C exposure during pregnancy regulates TNFα, BDNF, and NGF expression in neonatal brain and the maternal–fetal unit of the rat

Gilmore, John H., Jarskog, L. Fredrik, Vadlamudi, Swarooparani·2005·Journal of Neuroimmunology

Abstract

Maternal infection during pregnancy is associated with increased risk for neurodevelopmental disorders. Polyriboinosinic-polyribocytidilic acid (poly I:C) or saline was administered to rats to model maternal infection; levels of TNFalpha, brain-derived neurotrophic factor (BDNF), and nerve growth factor (NGF) were determined by ELISA. TNFalpha was significantly increased in maternal plasma, placenta, and amniotic fluid, while it was significantly decreased in fetal liver/spleen and neonatal brain. NGF and BDNF were significantly decreased in the placenta and fetal liver/spleen. There was no change in BDNF or NGF in the fetal or neonatal brain. Changes in TNFalpha, BDNF, and NGF after maternal exposure to poly I:C represent a potential mechanism through which maternal infection increases risk for neurodevelopmental disorders.

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Crossref · 10.1016/j.jneuroim.2004.10.008

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  • 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 Gilmore et al, 2005

  • 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 Gilmore et al, 2005

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Authors
Gilmore, J. H., Jarskog, L. F., & Vadlamudi, S.
Affiliations
University of North Carolina at Chapel Hill (US)
Corresponding author
Gilmore, John H.
Venue
Journal of Neuroimmunology
Publisher
Elsevier BV
Published
2005-02
Volume
159
Issue
1-2
Pages
106-112
ISSN
0165-5728 (ISSN-L)
OpenAlex
W1989871271
Cited by
177
References
40
Citations by year
2026: 1 · 2025: 2 · 2024: 6 · 2023: 7 · 2022: 6 · 2021: 5 · 2020: 12 · 2019: 5 · 2018: 12 · 2017: 8 · 2016: 3 · 2015: 15 · 2014: 8 · 2013: 8 · 2012: 16
FWCI
2.22
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neuroimmunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Mental Health (MH-60352, R01MH060352)
Topics
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
Keywords
maternal infection, poly(I:C), pregnancy, TNF-α, brain-derived neurotrophic factor, nerve growth factor, neurotrophins, neonatal brain, placenta, amniotic fluid, neurodevelopmental disorders, neuroinflammation
MeSH terms
Amniotic Fluid, Animals, Animals, Newborn, Brain, Female, Injections, Intraperitoneal, Liver, Maternal-Fetal Exchange, Poly I-C, Pregnancy, Pregnancy Proteins, Prenatal Exposure Delayed Effects, Spleen, Tumor Necrosis Factor-alpha, Down-Regulation, Up-Regulation, Rats, Sprague-Dawley, Maternal Exposure, Brain-Derived Neurotrophic Factor, Nerve Growth Factor, Rats

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