Evidence map›Paper›PMID 24485491›Full record

ArticlePsychoneuroendocrinology2014

Chronic exposure to exogenous glucocorticoids primes microglia to pro-inflammatory stimuli and induces NLRP3 mRNA in the hippocampus.

Matthew G Frank, Sarah A Hershman, Michael D Weber, Linda R Watkins, Steven F Maier

Abstract read
In one paragraph

Article in Psychoneuroendocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 1 pooled it
8.1field-weighted citation impact, top 2% 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

94 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Rethinking Corticosteroid Therapy in Pediatric Neurology.Journal of inflammation research · 2026
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34 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Matthew G FrankDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado, Boulder, CO, USA. Electronic address: matt.frank@colorado.edu.
Sarah A HershmanDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado, Boulder, CO, USA.
Michael D WeberDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado, Boulder, CO, USA.
Linda R WatkinsDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado, Boulder, CO, USA.
Steven F MaierDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado, Boulder, CO, USA.
University of Colorado Boulder · US

Funding

Preventing Transition of Acute-to-Chronic Neuropathic Pain: Models, Mechanisms &R01DE021966 · NIDCR · UNIVERSITY OF COLORADO · PI BARTH, DANIEL S., FLESHNER, MONIKA · 2011 to 2015
$2.0M
Stress, Glucocorticoids and Neuroinflammatory PrimingR21MH096224 · NIMH · UNIVERSITY OF COLORADO · PI MAIER, STEVEN F · 2012 to 2013
$400k
NIDCR NIH HHS R01 DE021966NIMH NIH HHS R21 MH096224NIMH NIH HHS R21MH096224
6 · The paper itself

Abstract

Chronic stress as well as chronic treatment with glucocorticoids (GCs) primes the neuroinflammatory response to a subsequent pro-inflammatory challenge. However, it remains unclear whether chronic GCs sensitize the response of key CNS immune substrates (i.e. microglia) to pro-inflammatory stimuli. In the present set of studies, male Sprague-Dawley rats underwent sham surgery or were adrenalectomized and then treated with varying concentrations of corticosterone (CORT; 0, 25, 50, and 75 μg/ml) administered in their drinking water. After 10 days of CORT exposure, whole hippocampus was collected and expression of glial activation markers measured or hippocampal microglia were isolated and challenged with LPS to probe for CORT-induced sensitization of pro-inflammatory responses. Chronic CORT exposure increased the gene expression of NLRP3, Iba-1, MHCII, and NF-κBIα in a concentration dependent manner. Chronic CORT (75 μg/ml) exposure potentiated the microglial proinflammatory response (TNFα, IL-1β, IL-6 and NLRP3) to LPS compared to the microglial response of sham surgery animals treated with vehicle. The present set of results demonstrate that chronic exposure to GCs primes microglia to pro-inflammatory stimuli and add to a growing body of evidence suggesting that a permissive function of GCs is that of an endogenous danger signal or alarmin.

Indexed as

AnimalsCarrier ProteinsCytokinesDrug SynergismGlucocorticoidsHippocampusInflammation MediatorsLipopolysaccharidesMaleMicrogliaNLR Family, Pyrin Domain-Containing 3 ProteinRatsRats, Sprague-DawleyReceptors, Cytoplasmic and NuclearStress, PsychologicalTime FactorsCarrier ProteinsCytokinesGlucocorticoidsInflammation MediatorsLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratReceptors, Cytoplasmic and NuclearGlucocorticoidsInflammasomeMicrogliaNeuroinflammationPrimingStress

Identifiers

PMID24485491
PMCPMC3912460
OpenAlexW1993894887

What OpenQuestion holds

Textmetadata
LicenceTDM
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.