Evidence map›Paper›PMID 30737481›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2019

Early life alcohol exposure primes hypothalamic microglia to later-life hypersensitivity to immune stress: possible epigenetic mechanism.

Lucy G Chastain, Tina Franklin, Omkaram Gangisetty, Miguel A Cabrera, Sayani Mukherjee, Pallavi Shrivastava, Shaima Jabbar, Dipak K Sarkar

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
12.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
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  4. Disrupted maternal care alters neural-microglia interactions in the primate paralaminar (PL) nucleus of the amygdala.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  5. Article
  6. Review
  7. Prenatal Alcohol Exposure and Mitochondrial Function in the Brain.Advances in experimental medicine and biology · 2026
    Review
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  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Lucy G ChastainThe Endocrine Program, Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.
Tina FranklinThe Endocrine Program, Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.
Omkaram GangisettyThe Endocrine Program, Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.
Miguel A CabreraThe Endocrine Program, Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.
Sayani MukherjeeThe Endocrine Program, Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.
Pallavi ShrivastavaThe Endocrine Program, Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.
Shaima JabbarThe Endocrine Program, Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA.
Dipak K SarkarThe Endocrine Program, Department of Animal Sciences, Rutgers, The State University of New Jersey, New Brunswick, NJ, USA. sarkar@aesop.rutgers.edu.
Rutgers, The State University of New Jersey · US

Funding

UMDNJ-RUTGERS UNIVERSITY PIPELINE PROGRAMR25GM055145 · NIGMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI HAIMOVICH, BEATRICE, LANGER, JEROME ALAN · 1996 to 2020
$8.7M
Role of Opiates in Alcohol-Induced Neurotoxicity- Diversity supplementR37AA008757 · NIAAA · RUTGERS, THE STATE UNIV OF N.J. · PI SARKAR, DIPAK KUMAR · 2009 to 2018
$4.0M
Microglial opioid receptor regulation of HPA axis disruption by neonatal alcoholF32AA023434 · NIAAA · RUTGERS, THE STATE UNIV OF N.J. · PI CHASTAIN, LUCY GUILLORY · 2015 to 2017
$149k
NIAAA NIH HHS F32 AA023434NIAAA NIH HHS R37 AA008757NIGMS NIH HHS R25 GM055145
6 · The paper itself

Abstract

Growing evidence has shown that developmental alcohol exposure induces central nervous system inflammation and microglia activation, which may contribute to long-term health conditions, such as fetal alcohol spectrum disorders. These studies sought to investigate whether neonatal alcohol exposure during postnatal days (PND) 2-6 in rats (third trimester human equivalent) leads to long-term disruption of the neuroimmune response by microglia. Exposure to neonatal alcohol resulted in acute increases in activation and inflammatory gene expression in hypothalamic microglia including tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6). Adults with neonatal alcohol pre-exposure (alcohol fed; AF) animals showed an exaggerated peripheral stress hormonal response to an immune challenge (lipopolysaccharides; LPS). In addition, there were significantly more microglia present in the hypothalamus of adult AF animals, and their hypothalamic microglia showed more cluster of differentiation molecule 11b (Cd11b) activation, TNF-α expression, and IL-6 expression in response to LPS. Interestingly, blocking microglia activation with minocycline treatment during PND 2-6 alcohol exposure ameliorated the hormonal and microglial hypersensitivity to LPS in AF adult animals. Investigation of possible epigenetic programming mechanisms by alcohol revealed neonatal alcohol decreased several repressive regulators of transcription in hypothalamic microglia, while concomitantly increasing histone H3 acetyl lysine 9 (H3K9ac) enrichment at TNF-α and IL-6 promoter regions. Importantly, adult hypothalamic microglia from AF animals showed enduring increases in H3K9ac enrichment of TNF-α and IL-6 promoters both at baseline and after LPS exposure, suggesting a possible epigenetic mechanism for the long-term immune disruption due to hypothalamic microglial priming.

Indexed as

AnimalsAnimals, NewbornCentral Nervous System DepressantsEpigenesis, GeneticEthanolGene ExpressionHistone CodeHypothalamusInflammationInterleukin-6LipopolysaccharidesMicrogliaRatsTumor Necrosis Factor-alphaCentral Nervous System DepressantsEthanolIl6 protein, ratInterleukin-6LipopolysaccharidesTumor Necrosis Factor-alpha

Identifiers

PMID30737481
PMCPMC6785096
OpenAlexW2913062637

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.