Evidence map›Paper›PMID 32485293›Full record

ArticleBrain, behavior, and immunity2020

Acute stress induces chronic neuroinflammatory, microglial and behavioral priming: A role for potentiated NLRP3 inflammasome activation.

Matthew G Frank, Laura K Fonken, Linda R Watkins, Steven F Maier

Open access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 59 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Matthew G FrankDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado Boulder, Boulder, CO 80301, USA. Electronic address: matt.frank@colorado.edu.
Laura K FonkenDivision of Pharmacology and Toxicology, University of Texas at Austin, Austin, TX 78712, USA.
Linda R WatkinsDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado Boulder, Boulder, CO 80301, USA.
Steven F MaierDepartment of Psychology and Neuroscience, Center for Neuroscience, University of Colorado Boulder, Boulder, CO 80301, USA.
University of Colorado Boulder · USThe University of Texas at Austin · US

Funding

Stress-induced neuroinflammatory priming: Glucocorticoids, inflammasomes, alarminsR01MH108523 · NIMH · UNIVERSITY OF COLORADO · PI MAIER, STEVEN F · 2016 to 2020
$2.1M
NIMH NIH HHS R01 MH108523
6 · The paper itself

Abstract

Prior exposure to acute and chronic stressors potentiates the neuroinflammatory and microglial pro-inflammatory response to subsequent immune challenges suggesting that stressors sensitize or prime microglia. Stress-induced priming of the NLRP3 inflammasome has been implicated in this priming phenomenon, however the duration/persistence of these effects has not been investigated. In the present study, we examined whether exposure to a single acute stressor (inescapable tailshock) induced a protracted priming of the NLRP3 inflammasome as well as the neuroinflammatory, behavioral and microglial proinflammatory response to a subsequent immune challenge in hippocampus. In male Sprague-Dawley rats, acute stress potentiated the neuroinflammatory response (IL-1β, IL-6, and NFκBIα) to an immune challenge (lipopolysaccharide; LPS) administered 8 days after stressor exposure. Acute stress also potentiated the proinflammatory cytokine response (IL-1β, IL-6, TNF and NFκBIα) to LPS ex vivo. This stress-induced priming of microglia also was observed 28 days post-stress. Furthermore, challenge with LPS reduced juvenile social exploration, but not sucrose preference, in animals exposed to stress 8 days prior to immune challenge. Exposure to acute stress also increased basal mRNA levels of NLRP3 and potentiated LPS-induction of caspase-1 mRNA and protein activity 8 days after stress. The present findings suggest that acute stress produces a protracted vulnerability to the neuroinflammatory effects of subsequent immune challenges, thereby increasing risk for stress-related psychiatric disorders with an etiological inflammatory component. Further, these findings suggest the unique possibility that acute stress might induce innate immune memory in microglia.

Indexed as

InflammasomesMicrogliaAnimalsLipopolysaccharidesMaleNLR Family, Pyrin Domain-Containing 3 ProteinRatsRats, Sprague-DawleyInflammasomesLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratInflammasomeMicrogliaNeuroinflammationNLRP3PrimingStress

Identifiers

PMID32485293
PMCPMC7572608
OpenAlexW3030963092

What OpenQuestion holds

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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.