Evidence map›Paper›PMID 30010986›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2018

In Vitro Transformation of Human Bronchial Epithelial Cells by Diesel Exhaust Particles: Gene Expression Profiling and Early Toxic Responses.

Iselin Rynning, Jiri Neca, Kristyna Vrbova, Helena Libalova, Pavel Rossner, Jørn A Holme, Kristine B Gützkow, Anani K Johnny Afanou, Yke J Arnoldussen, Eva Hruba and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. Air pollution-induced airway epithelial barrier dysfunction in COPD: a narrative review of mechanisms and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Role of air pollutants in airway epithelial barrier dysfunction in asthma and COPD.European respiratory review : an official journal of the European Respiratory Society · 2022
    Review
  8. Article
  9. Overexpression of Laminin 5Journal of oncology · 2022
    Article
  10. Article
  11. Environmental Epigenetics of Diesel Particulate Matter Toxicogenomics.International journal of environmental research and public health · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. PMFrontiers in physiology · 2019
    Review
  20. 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

15 authors at 4 institutions in 2 countries.

Iselin RynningSection for Toxicology and Biological Work Environment, Department of Chemical and Biological Work Environment, National Institute of Occupational Health, N-0304 Oslo, Norway.
Jiri NecaDepartment of Chemistry and Toxicology, Veterinary Research Institute, 621 00 Brno, Czech Republic.
Kristyna VrbovaDepartment of Genetic Toxicology and Nanotoxicology, Institute of Experimental Medicine of the Czech Academy of Sciences, 142 20 Prague, Czech Republic.
Helena LibalovaDepartment of Genetic Toxicology and Nanotoxicology, Institute of Experimental Medicine of the Czech Academy of Sciences, 142 20 Prague, Czech Republic.
Pavel RossnerDepartment of Genetic Toxicology and Nanotoxicology, Institute of Experimental Medicine of the Czech Academy of Sciences, 142 20 Prague, Czech Republic.
Jørn A HolmeDivision of Infection Control, Environment and Health, Department of Air and Noise.
Kristine B GützkowDivision of Infection Control, Department of Molecular Biology, Norwegian Institute of Public Health, N-0304 Oslo, Norway.
Anani K Johnny AfanouSection for Toxicology and Biological Work Environment, Department of Chemical and Biological Work Environment, National Institute of Occupational Health, N-0304 Oslo, Norway.
Yke J ArnoldussenSection for Toxicology and Biological Work Environment, Department of Chemical and Biological Work Environment, National Institute of Occupational Health, N-0304 Oslo, Norway.
Eva HrubaDepartment of Chemistry and Toxicology, Veterinary Research Institute, 621 00 Brno, Czech Republic.
Øivind SkareDepartment of Occupational Medicine and Epidemiology, National Institute of Occupational Health, N-0304 Oslo, Norway.
Aage HaugenSection for Toxicology and Biological Work Environment, Department of Chemical and Biological Work Environment, National Institute of Occupational Health, N-0304 Oslo, Norway.
Jan TopinkaDepartment of Genetic Toxicology and Nanotoxicology, Institute of Experimental Medicine of the Czech Academy of Sciences, 142 20 Prague, Czech Republic.
Miroslav MachalaDepartment of Chemistry and Toxicology, Veterinary Research Institute, 621 00 Brno, Czech Republic.
Steen MollerupSection for Toxicology and Biological Work Environment, Department of Chemical and Biological Work Environment, National Institute of Occupational Health, N-0304 Oslo, Norway.
National Institute of Occupational Health · NOCzech Academy of Sciences, Institute of Experimental Medicine · CZVeterinary Research Institute · CZNorwegian Institute of Public Health · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Occupational exposure to diesel exhaust may cause lung cancer in humans. Mechanisms include DNA-damage and inflammatory responses. Here, the potential of NIST SRM2975 diesel exhaust particles (DEP) to transform human bronchial epithelial cells (HBEC3) in vitro was investigated. Long-term exposure of HBEC3 to DEP led to increased colony growth in soft agar. Several DEP-transformed cell lines were established and based on the expression of epithelial-to-mesenchymal-transition (EMT) marker genes, one of them (T2-HBEC3) was further characterized. T2-HBEC3 showed a mesenchymal/fibroblast-like morphology, reduced expression of CDH1, and induction of CDH2 and VIM. T2-HBEC3 had reduced migration potential compared with HBEC3 and little invasion capacity. Gene expression profiling showed baseline differences between HBEC3 and T2-HBEC3 linked to lung carcinogenesis. Next, to assess differences in sensitivity to DEP between parental HBEC3 and T2-HBEC3, gene expression profiling was carried out after DEP short-term exposure. Results revealed changes in genes involved in metabolism of xenobiotics and lipids, as well as inflammation. HBEC3 displayed a higher steady state of IL1B gene expression and release of IL-1β compared with T2-HBEC3. HBEC3 and T2-HBEC3 showed similar susceptibility towards DEP-induced genotoxic effects. Liquid-chromatography-tandem-mass-spectrometry was used to measure secretion of eicosanoids. Generally, major prostaglandin species were released in higher concentrations from T2-HBEC3 than from HBEC3 and several analytes were altered after DEP-exposure. In conclusion, long-term exposure to DEP-transformed human bronchial epithelial cells in vitro. Differences between HBEC3 and T2-HBEC3 regarding baseline levels and DEP-induced changes of particularly CYP1A1, IL-1β, PGE2, and PGF2α may have implications for acute inflammation and carcinogenesis.

Indexed as

Air PollutantsBronchiCell Culture TechniquesCell Line, TransformedDNA DamageEpithelial CellsEpithelial-Mesenchymal TransitionGene Expression ProfilingHumansInterleukin-1betaParticulate MatterTranscriptomeVehicle EmissionsAir PollutantsInterleukin-1betaParticulate MatterVehicle Emissions

Identifiers

PMID30010986
PMCPMC6204768
OpenAlexW2883374375

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.