Evidence map›Paper›PMID 30463579›Full record

ArticleJournal of neuroinflammation2018

STING-mediated type-I interferons contribute to the neuroinflammatory process and detrimental effects following traumatic brain injury.

Amar Abdullah, Moses Zhang, Tony Frugier, Sammy Bedoui, Juliet M Taylor, Peter J Crack

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

107 citing papers in PubMed, 162 citations in OpenAlex.

  1. Article
  2. [Mechanisms of cGAS-STING-mediated chronic inflammation and targeted interventions in brain aging].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Review
  3. [Mechanisms of cGAS-STING signaling pathway mediated neuroinflammation in central nervous system and their therapeutic implications].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Review
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  12. CSF1R and IL1R1 inhibitors synergistically attenuate the early pathogenesis of traumatic brain injury in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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47 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

6 authors at 2 institutions in 1 country.

Amar AbdullahNeuropharmacology Laboratory, Department of Pharmacology & Therapeutics, University of Melbourne, Parkville, Melbourne, 3010, Australia.
Moses ZhangNeuropharmacology Laboratory, Department of Pharmacology & Therapeutics, University of Melbourne, Parkville, Melbourne, 3010, Australia.
Tony FrugierNeuropharmacology Laboratory, Department of Pharmacology & Therapeutics, University of Melbourne, Parkville, Melbourne, 3010, Australia.
Sammy BedouiDepartment of Microbiology & Immunology, Peter Doherty Institute, Melbourne, 3010, Australia.
Juliet M TaylorNeuropharmacology Laboratory, Department of Pharmacology & Therapeutics, University of Melbourne, Parkville, Melbourne, 3010, Australia. juliett@unimelb.edu.au.ORCID http://orcid.org/0000-0002-4596-6760
Peter J CrackNeuropharmacology Laboratory, Department of Pharmacology & Therapeutics, University of Melbourne, Parkville, Melbourne, 3010, Australia. pcrack@unimelb.edu.au.
The University of Melbourne · AUPeter Doherty Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTraumatic brain injury (TBI) represents a major cause of disability and death worldwide with sustained neuroinflammation and autophagy dysfunction contributing to the cellular damage. Stimulator of interferon genes (STING)-induced type-I interferon (IFN) signalling is known to be essential in mounting the innate immune response against infections and cell injury in the periphery, but its role in the CNS remains unclear. We previously identified the type-I IFN pathway as a key mediator of neuroinflammation and neuronal cell death in TBI. However, the modulation of the type-I IFN and neuroinflammatory responses by STING and its contribution to autophagy and neuronal cell death after TBI has not been explored.

methodsC57BL/6J wild-type (WT) and STING

resultsA significant upregulation in STING expression was identified in late trauma human brain samples that was confirmed in wild-type mice at 2 h and 24 h after CCI. This correlated with an elevated pro-inflammatory cytokine profile with increased TNF-α, IL-6, IL-1β and type-I IFN (IFN-α and IFN-β) levels. This expression was suppressed in the STING

conclusionOur data implicates a detrimental role for STING in mediating the TBI-induced neuroinflammatory response and autophagy dysfunction, potentially identifying a new therapeutic target for reducing cellular damage in TBI.

Indexed as

AnimalsAutophagyBrainBrain Injuries, TraumaticCalcium-Binding ProteinsCytokinesDisease Models, AnimalEncephalitisFunctional LateralityGene Expression RegulationGlial Fibrillary Acidic ProteinHepatocyte Nuclear Factor 3-alphaHumansLysosomal-Associated Membrane Protein 2MaleMembrane ProteinsAif1 protein, mouseCalcium-Binding ProteinsCytokinesFoxa1 protein, mouseGlial Fibrillary Acidic ProteinHepatocyte Nuclear Factor 3-alphaLysosomal-Associated Membrane Protein 2Membrane ProteinsMicrofilament ProteinsNerve Tissue ProteinsSting1 protein, mouseSTING ProteinAutophagyNeuroinflammationSTINGTraumatic brain injuryType-I interferon

Identifiers

PMID30463579
PMCPMC6247615
OpenAlexW2900778412

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.