Evidence map›Paper›PMID 32383538›Full record

ArticleEMBO reports2020

Glucocorticoids limit lipopolysaccharide-induced lethal inflammation by a double control system.

Kelly Van Looveren, Steven Timmermans, Tineke Vanderhaeghen, Charlotte Wallaeys, Marlies Ballegeer, Jolien Souffriau, Melanie Eggermont, Jolien Vandewalle, Lise Van Wyngene, Karolien De Bosscher and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

16 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
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  5. Article
  6. Effect ofBiomolecules & biomedicine · 2024
    Article
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  15. Article
  16. Glucocorticoids in Sepsis: To Be or Not to Be.Frontiers in immunology · 2020
    Review
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

11 authors at 1 institution in 1 country.

Kelly Van LooverenVIB Center for Inflammation Research, Ghent, Belgium.
Steven TimmermansVIB Center for Inflammation Research, Ghent, Belgium.
Tineke VanderhaeghenVIB Center for Inflammation Research, Ghent, Belgium.
Charlotte WallaeysVIB Center for Inflammation Research, Ghent, Belgium.
Marlies BallegeerVIB Center for Inflammation Research, Ghent, Belgium.
Jolien SouffriauVIB Center for Inflammation Research, Ghent, Belgium.
Melanie EggermontVIB Center for Inflammation Research, Ghent, Belgium.
Jolien VandewalleVIB Center for Inflammation Research, Ghent, Belgium.ORCID 0000-0003-1844-6476
Lise Van WyngeneVIB Center for Inflammation Research, Ghent, Belgium.ORCID 0000-0002-9078-0113
Karolien De BosscherDepartment of Biochemistry, Ghent University, Ghent, Belgium.
Claude LibertVIB Center for Inflammation Research, Ghent, Belgium.ORCID 0000-0001-6408-036X
Ghent University · BE

Funding

Fonds Wetenschappelijk Onderzoek (FWO) G006616NUniversiteit Gent (UGent) BOF19-GOA-004-1Vlaams Instituut voor Biotechnologie (VIB) DOTATION-LIBERT-2017-2021
6 · The paper itself

Abstract

Lipopolysaccharides (LPS) can lead to a lethal endotoxemia, which is a systemic inflammatory response syndrome (SIRS) characterized by a systemic release of cytokines, such as TNF. Endotoxemia is studied intensely, as a model system of Gram-negative infections. LPS- and TNF-induced SIRS involve a strong induction of interferon-stimulated genes (ISGs), some of which cause cell death in the intestinal epithelium cells (IECs). It is well known that glucocorticoids (GCs) protect against endotoxemia. By applying numerous mutant mouse lines, our data support a model whereby GCs, via their glucocorticoid receptor (GR), apply two key mechanisms to control endotoxemia, (i) at the level of suppression of TNF production in a GR monomer-dependent way in macrophages and (ii) at the level of inhibition of TNFR1-induced ISG gene expression and necroptotic cell death mediators in IECs in a GR dimer-dependent way. Our data add new important insights to the understanding of the role of TNF in endotoxemia and the two separate key roles of GCs in suppressing TNF production and activity.

Indexed as

EndotoxemiaLipopolysaccharidesAnimalsCytokinesGlucocorticoidsInflammationMiceTumor Necrosis Factor-alphaCytokinesGlucocorticoidsLipopolysaccharidesTumor Necrosis Factor-alphaglucocorticoidslipopolysaccharidessystemic inflammatory response syndromeTNF

Identifiers

PMID32383538
PMCPMC7332980
OpenAlexW3023695562

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.