Evidence map›Paper›PMID 29768427›Full record

ArticlePloS one2018

Differential effects of TNF-α and IL-1β on the control of metal metabolism and cadmium-induced cell death in chronic inflammation.

Paola Bonaventura, Aline Lamboux, Francis Albarède, Pierre Miossec

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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  19. Anti-Inflammation Associated Protective Mechanism of Berberine and its Derivatives on Attenuating Pentylenetetrazole-Induced Seizures in Zebrafish.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
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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.

Paola BonaventuraDepartment of Immunology and Rheumatology, Immunogenomics and Inflammation Research Unit EA 4130, University of Lyon, Edouard Herriot Hospital, Lyon, France.
Aline LambouxGeology Laboratory-Department of Earth Sciences, Ecole Normale Supérieure de Lyon and CNRS Lyon, France.
Francis AlbarèdeGeology Laboratory-Department of Earth Sciences, Ecole Normale Supérieure de Lyon and CNRS Lyon, France.
Pierre MiossecDepartment of Immunology and Rheumatology, Immunogenomics and Inflammation Research Unit EA 4130, University of Lyon, Edouard Herriot Hospital, Lyon, France.ORCID 0000-0002-3280-6346
École Normale Supérieure de Lyon · FRUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveInterleukin-1-beta (IL-1β) and tumour necrosis factor-alpha (TNF-α) are both monocyte-derived cytokines. Both cytokines have been previously described to exert a role in rheumatoid arthritis (RA) pathogenesis synergizing with other pro-inflammatory mediators, such as interleukin-17 (IL-17) on target cells, for the perpetuation of the inflammatory response (e.g. IL-6 production). In the context of experimental RA, Cd addition has an anti-proliferative and anti-inflammatory effect when associated to IL-17/TNF-α stimulation, due to its accumulation in synoviocytes. The aim of this work was to evaluate if IL-1β interaction with IL-17 also contributes to metal-import mechanisms and its effects on cell viability and inflammation.

methodsIL-17 and IL-1β were added to synoviocyte cultures with or without exogenous Cd addition (0.1 ppm, 0.89 μM). IL-6 production, Cd import kinetics, gene expression of ZIP-8 importer and metallothioneins (MTs) and cell viability were evaluated by ELISA, inductively-coupled mass spectrometry (ICP-MS), q-RT-PCR and viability assays (neutral red and annexin V) respectively.

resultsIL-17 and IL-1β acted in synergy on synoviocytes to induce IL-6 production similarly to the IL-17/TNF-α combination. Metal import was lower with IL17/ IL-1β in comparison to IL-17/TNF-α exposed-synoviocytes, as the expression of ZIP-8 and MT-1F was less induced. Monocyte and PBMCs exposure to Cd resulted in a reduced production of IL-1β and an increased production of TNF-α and this result was confirmed in co-cultures of synoviocytes and PBMCs. The IL-17/IL-1β combination with Cd slightly reduced cell viability in comparison to the IL-17/TNF-α combination and resulted in a strong induction of IL-6 production.

conclusionIL-17/TNF-α combination but not IL-17/IL-1β combination mainly drives the accumulation of Cd in synoviocytes and its effects on cell viability and inflammation.

Indexed as

Arthritis, RheumatoidBiological Transport, ActiveCadmiumCell DeathCells, CulturedHumansInflammationInflammation MediatorsInterleukin-17Interleukin-1betaInterleukin-6MonocytesSignal TransductionSynoviocytesTumor Necrosis Factor-alphaCadmiumIL6 protein, humanInflammation MediatorsInterleukin-17Interleukin-1betaInterleukin-6Tumor Necrosis Factor-alpha

Identifiers

PMID29768427
PMCPMC5955583
OpenAlexW2804722531

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.