Evidence map›Paper›PMID 31206650›Full record

ArticleEuropean journal of immunology2019

Bromodomain inhibitor I-BET151 suppresses immune responses during fungal-immune interaction.

Jorge Domínguez-Andrés, Anaísa V Ferreira, Trees Jansen, Nicholas Smithers, Rab K Prinjha, Rebecca C Furze, Mihai G Netea

Open access · hybridAbstract read
In one paragraph

Article in European journal of immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

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  14. The BET family in immunity and disease.Signal transduction and targeted therapy · 2021
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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

7 authors at 5 institutions in 5 countries.

Jorge Domínguez-AndrésDepartment of Internal Medicine and Radboud Center for Infectious diseases (RCI), Radboud University Nijmegen Medical Centre, 6500HB, Nijmegen, the Netherlands.
Anaísa V FerreiraDepartment of Internal Medicine and Radboud Center for Infectious diseases (RCI), Radboud University Nijmegen Medical Centre, 6500HB, Nijmegen, the Netherlands.
Trees JansenDepartment of Internal Medicine and Radboud Center for Infectious diseases (RCI), Radboud University Nijmegen Medical Centre, 6500HB, Nijmegen, the Netherlands.
Nicholas SmithersEpigenetics DPU, Immuno-Inflammation Therapy Area, GlaxoSmithKline R&D, Medicines Research Centre, Stevenage, SG1 2NY, UK.
Rab K PrinjhaEpigenetics DPU, Immuno-Inflammation Therapy Area, GlaxoSmithKline R&D, Medicines Research Centre, Stevenage, SG1 2NY, UK.
Rebecca C FurzeEpigenetics DPU, Immuno-Inflammation Therapy Area, GlaxoSmithKline R&D, Medicines Research Centre, Stevenage, SG1 2NY, UK.
Mihai G NeteaDepartment of Internal Medicine and Radboud Center for Infectious diseases (RCI), Radboud University Nijmegen Medical Centre, 6500HB, Nijmegen, the Netherlands.
GlaxoSmithKline (United Kingdom) · GBRadboud University Nijmegen · NLAge UK · GBUniversidade do Porto · PTUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Changes in the epigenetic landscape of immune cells are a crucial component of gene activation during the induction of inflammatory responses, therefore it has been hypothesized that epigenetic modulation could be employed to restore homeostasis in inflammatory scenarios. Fungal pathogens cause a large burden of morbidity and even mortality due to the hyperinflammatory processes that induce mucosal, allergic or systemic infections. Bromodomain and extraterminal domain (BET) proteins are considered as one as the most tantalizing pharmacological targets for the modulation of inflammatory responses at the epigenetic level. Nothing is known of the role of BET inhibitors on the inflammation induced by fungal pathogens. In the present study, we assessed the in vitro efficacy of the small molecular histone mimic BET inhibitor I-BET151 to modulate innate immune responses during fungal-immune interaction with the clinically relevant fungal pathogens Candida albicans and Aspergillus fumigatus. Our results prove that BET inhibitors (I-BETs) represent an important modulator of inflammation induced by fungal pathogens: both direct production of proinflammatory cytokines and the induction of trained immunity were inhibited by I-BET151. These modulatory effects are likely to have important potential implications in clinically relevant situations.

Indexed as

Aspergillus fumigatusCandida albicansEndocytosisGene Expression RegulationHeterocyclic Compounds, 4 or More RingsHost-Pathogen InteractionsHumansImmunologic FactorsInterferon-gammaInterleukin-10Interleukin-17Interleukin-1betaInterleukin-22Interleukin-6Interleukin-6 InhibitorsInterleukinsGSK1210151AHeterocyclic Compounds, 4 or More RingsIL10 protein, humanIL1B protein, humanIL6 protein, humanImmunologic FactorsInterferon-gammaInterleukin-10Interleukin-17Interleukin-1betaInterleukin-22Interleukin-6Interleukin-6 InhibitorsInterleukinsTumor Necrosis Factor-alphaAspergillus fumigatusCandida albicansI-BET151monocytesneutrophils

Identifiers

PMID31206650
PMCPMC6899658
OpenAlexW2953241467

What OpenQuestion holds

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Registered trials

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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.