Evidence map›Paper›PMID 22649552›Full record

ArticlePloS one2012

Inflammasome-mediated IL-1β production in humans with cystic fibrosis.

Anthony Tang, Ashish Sharma, Roger Jen, Aaron F Hirschfeld, Mark A Chilvers, Pascal M Lavoie, Stuart E Turvey

Open access · goldAbstract readComparative Study
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 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. Normalization of Muc5b ameliorates airway mucus plugging during persistentAmerican journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  4. Frontiers in immunology · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Immunometabolism in biofilm infection: lessons from cancer.Molecular medicine (Cambridge, Mass.) · 2022
    Review
  11. Article
  12. Article
  13. Airway Inflammation and Host Responses in the Era of CFTR Modulators.International journal of molecular sciences · 2020
    Review
  14. 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

7 authors at 3 institutions in 1 country.

Anthony TangDepartment of Microbiology & Immunology, University of British Columbia, Vancouver, British Columbia, Canada.
Ashish Sharma
Roger Jen
Aaron F Hirschfeld
Mark A Chilvers
Pascal M Lavoie
Stuart E Turvey
University of British Columbia · CAChild and Family Research Institute · CABC Children's Hospital · CA

Funding

CIHR 123478-1
6 · The paper itself

Abstract

backgroundInflammation and infection are major determinants of disease severity and consequently, the quality of life and outcome for patients with cystic fibrosis (CF). Interleukin-1 beta (IL-1β) is a key inflammatory mediator. Secretion of biologically active IL-1β involves inflammasome-mediated processing. Little is known about the contribution of IL-1β and the inflammasomes in CF inflammatory disease. This study examines inflammasome-mediated IL-1β production in CF bronchial epithelial cell lines and human patients with CF.

resultsBronchial epithelial cell lines were found to produce negligible amounts of basal or stimulated IL-1β compared to hematopoeitic cells and they did not significantly upregulate caspase-1 activity upon inflammasome stimulation. In contrast, peripheral blood mononuclear cells (PBMCs) from both CF and healthy control subjects produced large amounts of IL-1β and strongly upregulated caspase-1 activity upon inflammasome stimulation. PBMCs from CF patients and controls displayed similar levels of caspase-1 activation and IL-1β production when stimulated with inflammasome activators. This IL-1β production was dependent on NF-κB activity and could be enhanced by priming with LPS. Finally, chemical inhibition of CFTR activity in control PBMCs and THP-1 cells did not significantly alter IL-1β or IL-8 production in response to P. aeruginosa.

conclusionHematopoeitic cells appear to be the predominant source of inflammasome-induced pro-inflammatory IL-1β in CF. PBMCs derived from CF subjects display preserved inflammasome activation and IL-1β secretion in response to the major CF pathogen Pseudomonas aeruginosa. However, our data do not support the hypothesis that increased IL-1β production in CF subjects is due to an intrinsic increase in NF-κB activity through loss of CFTR function.

Indexed as

Analysis of VarianceCaspasesCell LineCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorEpithelial CellsGene Expression RegulationHumansImmunoblottingInflammasomesInterleukin-1betaInterleukin-8Leukocytes, MononuclearNF-kappa BPseudomonas aeruginosaPseudomonas InfectionsCaspasesCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorInflammasomesInterleukin-1betaInterleukin-8NF-kappa B

Identifiers

PMID22649552
PMCPMC3359311
OpenAlexW1965741201

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.