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Corticosteroid effects on cell signalling.

P J Barnes1

  • 1Dept of Thoracic Medicine, National Heart and Lung Institute, Dovehouse St, London, SW3 6LY, UK. p.j.barnes@imperial.ac.uk

The European Respiratory Journal
|February 3, 2006
PubMed
Summary
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Corticosteroids treat asthma by reversing histone acetylation and activating anti-inflammatory genes. Impaired histone deacetylase 2 in smokers with asthma or COPD causes steroid resistance.

Area of Science:

  • Molecular Biology
  • Immunology
  • Pharmacology

Background:

  • Asthma inflammation involves gene expression regulated by transcription factors like NF-κB and AP-1.
  • Corticosteroids are primary anti-inflammatory asthma treatments.
  • Glucocorticoid receptors (GRs) mediate corticosteroid effects by modulating gene transcription.

Purpose of the Study:

  • To elucidate the molecular mechanisms of corticosteroid action in asthma.
  • To investigate the role of histone acetylation and deacetylation in corticosteroid sensitivity.
  • To explore reasons for steroid resistance in certain asthma and COPD patient groups.

Main Methods:

  • Analysis of gene expression and transcription factor activity in asthma models.
  • Investigation of glucocorticoid receptor (GR) binding and coactivator/corepressor recruitment.

Related Experiment Videos

  • Assessment of histone deacetylase 2 (HDAC2) activity and its regulation by oxidative stress.

    • Main Results:

    • Corticosteroids suppress inflammatory genes by reversing histone acetylation via GR-mediated recruitment of HDAC2.
    • Activated GRs can also induce anti-inflammatory gene transcription (e.g., MKP-1).
    • Impaired HDAC2 due to oxidative/nitrative stress in smokers with asthma/COPD leads to corticosteroid resistance.

    Conclusions:

    • Corticosteroids exert anti-inflammatory effects through epigenetic modifications involving histone acetylation.
    • Dysregulation of GR signaling or HDAC2 impairment compromises corticosteroid efficacy.
    • Targeting HDAC2 or mitigating oxidative stress may overcome steroid resistance in specific patient populations.