Evidence map›Paper›PMID 21827450›Full record

Trial reportBritish journal of pharmacology2012

Corticosteroid-induced gene expression in allergen-challenged asthmatic subjects taking inhaled budesonide.

M M Kelly, E M King, C F Rider, C Gwozd, N S Holden, J Eddleston, B Zuraw, R Leigh, P M O'Byrne, R Newton

Abstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Airway Smooth Muscle-Specific Transcriptomic Signatures of Glucocorticoid Exposure.American journal of respiratory cell and molecular biology · 2019
    Article
  11. Glucocorticoids and Airway Smooth Muscle: A Few More Answers, Still More Questions.American journal of respiratory cell and molecular biology · 2019
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Long-ActingMolecular pharmacology · 2018
    Article
  17. Article
  18. Article
  19. 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

10 authors at 3 institutions in 2 countries.

M M KellyAirways Inflammation Research Group, Institute of Infection, Immunity and Inflammation, Faculty of Medicine, University of Calgary, Calgary, AB, CanadaAllergy and Immunology Section, University of California, San Diego School of Medicine, La Jolla, CA, USAFirestone Institute for Respiratory Health, St. Joseph's Hospital and the Department of Medicine, McMaster University, Hamilton, ON, Canada.
E M KingAirways Inflammation Research Group, Institute of Infection, Immunity and Inflammation, Faculty of Medicine, University of Calgary, Calgary, AB, CanadaAllergy and Immunology Section, University of California, San Diego School of Medicine, La Jolla, CA, USAFirestone Institute for Respiratory Health, St. Joseph's Hospital and the Department of Medicine, McMaster University, Hamilton, ON, Canada.
C F RiderAirways Inflammation Research Group, Institute of Infection, Immunity and Inflammation, Faculty of Medicine, University of Calgary, Calgary, AB, CanadaAllergy and Immunology Section, University of California, San Diego School of Medicine, La Jolla, CA, USAFirestone Institute for Respiratory Health, St. Joseph's Hospital and the Department of Medicine, McMaster University, Hamilton, ON, Canada.
C GwozdAirways Inflammation Research Group, Institute of Infection, Immunity and Inflammation, Faculty of Medicine, University of Calgary, Calgary, AB, CanadaAllergy and Immunology Section, University of California, San Diego School of Medicine, La Jolla, CA, USAFirestone Institute for Respiratory Health, St. Joseph's Hospital and the Department of Medicine, McMaster University, Hamilton, ON, Canada.
N S HoldenAirways Inflammation Research Group, Institute of Infection, Immunity and Inflammation, Faculty of Medicine, University of Calgary, Calgary, AB, CanadaAllergy and Immunology Section, University of California, San Diego School of Medicine, La Jolla, CA, USAFirestone Institute for Respiratory Health, St. Joseph's Hospital and the Department of Medicine, McMaster University, Hamilton, ON, Canada.
J EddlestonAirways Inflammation Research Group, Institute of Infection, Immunity and Inflammation, Faculty of Medicine, University of Calgary, Calgary, AB, CanadaAllergy and Immunology Section, University of California, San Diego School of Medicine, La Jolla, CA, USAFirestone Institute for Respiratory Health, St. Joseph's Hospital and the Department of Medicine, McMaster University, Hamilton, ON, Canada.
B ZurawAirways Inflammation Research Group, Institute of Infection, Immunity and Inflammation, Faculty of Medicine, University of Calgary, Calgary, AB, CanadaAllergy and Immunology Section, University of California, San Diego School of Medicine, La Jolla, CA, USAFirestone Institute for Respiratory Health, St. Joseph's Hospital and the Department of Medicine, McMaster University, Hamilton, ON, Canada.
R LeighAirways Inflammation Research Group, Institute of Infection, Immunity and Inflammation, Faculty of Medicine, University of Calgary, Calgary, AB, CanadaAllergy and Immunology Section, University of California, San Diego School of Medicine, La Jolla, CA, USAFirestone Institute for Respiratory Health, St. Joseph's Hospital and the Department of Medicine, McMaster University, Hamilton, ON, Canada.
P M O'ByrneAirways Inflammation Research Group, Institute of Infection, Immunity and Inflammation, Faculty of Medicine, University of Calgary, Calgary, AB, CanadaAllergy and Immunology Section, University of California, San Diego School of Medicine, La Jolla, CA, USAFirestone Institute for Respiratory Health, St. Joseph's Hospital and the Department of Medicine, McMaster University, Hamilton, ON, Canada.
R NewtonAirways Inflammation Research Group, Institute of Infection, Immunity and Inflammation, Faculty of Medicine, University of Calgary, Calgary, AB, CanadaAllergy and Immunology Section, University of California, San Diego School of Medicine, La Jolla, CA, USAFirestone Institute for Respiratory Health, St. Joseph's Hospital and the Department of Medicine, McMaster University, Hamilton, ON, Canada.
University of Calgary · CAUniversity of California, San Diego · USSt. Joseph's Hospital · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

background and purposeInhaled corticosteroids (ICS) are the cornerstone of asthma pharmacotherapy and, acting via the glucocorticoid receptor (GR), reduce inflammatory gene expression. While this is often attributed to a direct inhibitory effect of the GR on inflammatory gene transcription, corticosteroids also induce the expression of anti-inflammatory genes in vitro. As there are no data to support this effect in asthmatic subjects taking ICS, we have assessed whether ICS induce anti-inflammatory gene expression in subjects with atopic asthma. EXPERIMENTAL APPROACH: Bronchial biopsies from allergen-challenged atopic asthmatic subjects taking inhaled budesonide or placebo were subjected to gene expression analysis using real-time reverse transcriptase-PCR for the corticosteroid-inducible genes (official gene symbols with aliases in parentheses): TSC22D3 [glucocorticoid-induced leucine zipper (GILZ)], dual-specificity phosphatase-1 (MAPK phosphatase-1), both anti-inflammatory effectors, and FKBP5 [FK506-binding protein 51 (FKBP51)], a regulator of GR function. Cultured pulmonary epithelial and smooth muscle cells were also treated with corticosteroids before gene expression analysis. KEY

resultsCompared with placebo, GILZ and FKBP51 mRNA expression was significantly elevated in budesonide-treated subjects. Budesonide also increased GILZ expression in human epithelial and smooth muscle cells in culture. Immunostaining of bronchial biopsies revealed GILZ expression in the airways epithelium and smooth muscle of asthmatic subjects. CONCLUSIONS AND IMPLICATIONS: Expression of the corticosteroid-induced genes, GILZ and FKBP51, is up-regulated in the airways of allergen-challenged asthmatic subjects taking inhaled budesonide. Consequently, the biological effects of corticosteroid-induced genes should be considered when assessing the actions of ICS. Treatment modalities that increase or decrease GR-dependent transcription may correspondingly affect corticosteroid efficacy.

Indexed as

Administration, InhalationAdrenal Cortex HormonesAllergensAnti-Inflammatory AgentsAsthmaBronchodilator AgentsBudesonideCell Line, TumorCross-Over StudiesDual Specificity Phosphatase 1Epithelial CellsGene ExpressionHumansLungMyocytes, Smooth MuscleReverse Transcriptase Polymerase Chain ReactionAdrenal Cortex HormonesAllergensAnti-Inflammatory AgentsBronchodilator AgentsBudesonideDual Specificity Phosphatase 1RNA, MessengerTacrolimus Binding Protein 5Tacrolimus Binding ProteinsTranscription FactorsTSC22D3 protein, human

Identifiers

PMID21827450
PMCPMC3372826
OpenAlexW1495764983

What OpenQuestion holds

Textmetadata
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.