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Corticosteroid suppression of antiviral immunity increases bacterial loads and mucus production in COPD exacerbations

Aran Singanayagam1, Nicholas Glanville1, Jason L Girkin2

  • 1COPD and Asthma Section, National Heart and Lung Institute, Imperial College London, Norfolk Place, London, W2 1PG, UK.

Nature Communications
|June 10, 2018
PubMed

Insights

Inhaled corticosteroids impair immune responses to viruses in chronic obstructive pulmonary disease (COPD), increasing bacterial infections and mucus. Interferon-beta therapy may offer protection against these adverse effects.

Area of Science:

  • Immunology
  • Pulmonology
  • Microbiology

Background:

  • Inhaled corticosteroids (ICS) have limited efficacy in reducing chronic obstructive pulmonary disease (COPD) exacerbations and increase pneumonia risk via unknown mechanisms.
  • Rhinoviruses trigger most COPD exacerbations and heighten susceptibility to secondary bacterial infections.

Purpose of the Study:

  • To investigate the mechanisms by which ICS impact antiviral immunity and host defense during virus-induced COPD exacerbations.
  • To explore the potential of exogenous interferon-beta as a therapeutic intervention.

Main Methods:

  • Utilized a mouse model to study the effects of fluticasone propionate (FP), an ICS, on innate and acquired antiviral immune responses.
  • Investigated the role of type I interferon signaling in regulating mucus production and antibacterial immunity during rhinovirus infection.
  • Assessed the impact of exogenous interferon-beta administration on immune responses and clinical outcomes.

Main Results:

  • Fluticasone propionate (FP) was found to impair antiviral immune responses, leading to delayed virus clearance, increased mucus production, reduced antimicrobial peptide secretion, and elevated pulmonary bacterial load during virus-induced exacerbations.
  • Exogenous interferon-beta administration reversed these detrimental effects.
  • Mice lacking the type I interferon-α/β receptor (IFNAR1-/-) exhibited suppressed antimicrobial peptide responses and enhanced mucin production following rhinovirus infection.

Conclusions:

  • Type I interferon is identified as a critical regulator of antibacterial immunity and mucus production in the context of viral respiratory infections.
  • ICS-induced suppression of interferon during virus-induced COPD exacerbations likely contributes to pneumonia risk.
  • Inhaled interferon-beta therapy presents a potential protective strategy against exacerbations and associated complications in COPD patients.

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