Evidence map›Paper›PMID 28912506›Full record

ArticleScientific reports2017

Role of tumor necrosis factor-α and its receptors in diesel exhaust particle-induced pulmonary inflammation.

Smitha Kumar, Guy Joos, Louis Boon, Kurt Tournoy, Sharen Provoost, Tania Maes

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. 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
1.8field-weighted citation impact, top 17% 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, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Toll-Like Receptors/TNF-BioMed research international · 2022
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  8. Comparison of the Effects of Essential Oil Obtained from the Crude and Bran-ProcessedEvidence-based complementary and alternative medicine : eCAM · 2021
    Article
  9. Article
  10. Anti-Inflammatory Potentials of the n-Hexane Fraction ofJournal of inflammation research · 2021
    Article
  11. Article
  12. Review
  13. Article
  14. Dietary Supplementation with Sea Bass (International journal of molecular sciences · 2019
    Article
  15. Review
  16. Article
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 2 countries.

Smitha KumarLaboratory for Translational Research in Obstructive Pulmonary Diseases - Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
Guy JoosLaboratory for Translational Research in Obstructive Pulmonary Diseases - Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.ORCID 0000-0002-3149-9444
Louis BoonBioceros B.V., Utrecht, Netherlands.
Kurt TournoyLaboratory for Translational Research in Obstructive Pulmonary Diseases - Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.
Sharen ProvoostLaboratory for Translational Research in Obstructive Pulmonary Diseases - Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium. sharen.provoost@ugent.be.
Tania MaesLaboratory for Translational Research in Obstructive Pulmonary Diseases - Department of Respiratory Medicine, Ghent University Hospital, Ghent, Belgium.ORCID 0000-0002-3037-6928
Ghent University Hospital · BEPolpharma Biologics (Netherlands) · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhalation of diesel exhaust particles (DEP) induces an inflammatory reaction in the lung. However, the underlying mechanisms remain to be elucidated. Tumor necrosis factor alpha (TNF-α) is a pro-inflammatory cytokine that operates by binding to tumor necrosis factor receptor 1 (TNFR1) and tumor necrosis factor receptor 2 (TNFR2). The role of TNF-α signaling and the importance of either TNFR1 or TNFR2 in the DEP-induced inflammatory response has not yet been elucidated. TNF-α knockout (KO), TNFR1 KO, TNFR2 KO, TNFR1/TNFR2 double KO (TNFR-DKO) and wild type (WT) mice were intratracheally exposed to saline or DEP. Pro-inflammatory cells and cytokines were assessed in the bronchoalveolar lavage fluid (BALF). Exposure to DEP induced a dose-dependent inflammation in the BALF in WT mice. In addition, levels of TNF-α and its soluble receptors were increased upon exposure to DEP. The DEP-induced inflammation in the BALF was decreased in TNF-α KO, TNFR-DKO and TNFR2 KO mice. In contrast, the inflammatory response in the BALF of DEP-exposed TNFR1 KO mice was largely comparable with WT controls. In conclusion, these data provide evidence for a regulatory role of TNF-α in DEP-induced pulmonary inflammation and identify TNFR2 as the most important receptor in mediating these inflammatory effects.

Indexed as

Air PollutantsAnimalsBronchoalveolar Lavage FluidCytokinesDisease Models, AnimalInhalation ExposureLeukocytesMiceMice, KnockoutPneumoniaReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IITumor Necrosis Factor-alphaVehicle EmissionsAir PollutantsCytokinesReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IITumor Necrosis Factor-alphaVehicle Emissions

Identifiers

PMID28912506
PMCPMC5599628
OpenAlexW2754543786

What OpenQuestion holds

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LicenceCC BY
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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.