Evidence map›Paper›PMID 22363418›Full record

ArticlePloS one2012

Inflammatory transcriptome profiling of human monocytes exposed acutely to cigarette smoke.

William R Wright, Katarzyna Parzych, Damian Crawford, Charles Mein, Jane A Mitchell, Mark J Paul-Clark

Abstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–field-weighted citation impact
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

24 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. A crucial role of neutrophil extracellular traps in pulmonary infectious diseases.Chinese medical journal pulmonary and critical care medicine · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Metabolic Pathways and Networks Associated With Tobacco Use in Military Personnel.Journal of occupational and environmental medicine · 2016
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  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

6 authors.

William R WrightDepartment of Cardiothoracic Pharmacology, Pharmacology and Toxicology, National Heart and Lung Institute, Imperial College London, London, United Kingdom.
Katarzyna Parzych
Damian Crawford
Charles Mein
Jane A Mitchell
Mark J Paul-Clark

Funding

Wellcome TrustWellcome Trust 4627
6 · The paper itself

Abstract

backgroundCigarette smoking is responsible for 5 million deaths worldwide each year, and is a major risk factor for cardiovascular and lung diseases. Cigarette smoke contains a complex mixture of over 4000 chemicals containing 10(15) free radicals. Studies show smoke is perceived by cells as an inflammatory and xenobiotic stimulus, which activates an immune response. The specific cellular mechanisms driving cigarette smoke-induced inflammation and disease are not fully understood, although the innate immune system is involved in the pathology of smoking related diseases. METHODOLOGY/PRINCIPLE

findingsTo address the impact of smoke as an inflammagen on the innate immune system, THP-1 cells and Human PBMCs were stimulated with 3 and 10% (v/v) cigarette smoke extract (CSE) for 8 and 24 hours. Total RNA was extracted and the transcriptome analysed using Illumina BeadChip arrays. In THP-1 cells, 10% CSE resulted in 80 genes being upregulated and 37 downregulated by ≥1.5 fold after 8 hours. In PBMCs stimulated with 10% CSE for 8 hours, 199 genes were upregulated and 206 genes downregulated by ≥1.5 fold. After 24 hours, the number of genes activated and repressed by ≥1.5 fold had risen to 311 and 306 respectively. The major pathways that were altered are associated with cell survival, such as inducible antioxidants, protein chaperone and folding proteins, and the ubiquitin/proteosome pathway.

conclusionsOur results suggest that cigarette smoke causes inflammation and has detrimental effects on the metabolism and function of innate immune cells. In addition, THP-1 cells provide a genetically stable alternative to primary cells for the study of the effects of cigarette smoke on human monocytes.

Indexed as

Cell LineDatabases as TopicGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksHeme Oxygenase-1HumansInflammationInterleukin-8MonocytesPrincipal Component AnalysisSignal TransductionSmokingTumor Necrosis Factor-alphaCXCL8 protein, humanHeme Oxygenase-1HMOX1 protein, humanInterleukin-8Tumor Necrosis Factor-alpha

Identifiers

PMID22363418
PMCPMC3281820

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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.