Exogenous IFN-β has antiviral and anti-inflammatory properties in primary bronchial epithelial cells from asthmatic subjects exposed to rhinovirus

J Allergy Clin Immunol. 2011 May;127(5):1148-54.e9. doi: 10.1016/j.jaci.2011.01.023. Epub 2011 Feb 16.


Background: Rhinoviruses are the major cause of asthma exacerbations. Previous studies suggest that primary bronchial epithelial cells (PBECs) from asthmatic subjects are more susceptible to rhinovirus infection because of deficient IFN-β production. Although augmenting the innate immune response might provide a novel approach for treatment of virus-induced asthma exacerbations, the potential of IFN-β to modulate antiviral and proinflammatory responses in asthmatic epithelium is poorly characterized.

Objectives: We sought to compare responses of PBECs from nonasthmatic and asthmatic subjects to exogenous IFN-β and test the inflammatory effects of IFN-β in response to rhinovirus infection.

Methods: PBECs were treated with IFN-β and infected with a low inoculum of human rhinovirus serotype 1B to simulate a natural viral infection. Expression of interferon-responsive genes and inflammatory responses were analyzed by using reverse transcription-quantitative real-time PCR, cytometric bead arrays, or both; viral titers were assessed by using the 50% tissue culture infection dose.

Results: Expression of IFN-β-stimulated antiviral genes was comparable in PBECs from nonasthmatic or asthmatic donors. Exogenous IFN-β significantly protected PBECs from asthmatic donors against rhinovirus infection by suppressing viral replication. Interferon-inducible protein 10 (IP-10), RANTES, and IL-6 release in response to rhinovirus infection was triggered only in PBECs from asthmatic donors. Although exogenous IFN-β alone stimulated some release of IP-10 (but not IL-6 or RANTES), it significantly reduced rhinovirus-induced IP-10, RANTES, and IL-6 expression when tested in combination with rhinovirus.

Conclusions: PBECs from asthmatic donors have a normal antiviral response to exogenous IFN-β. The ability of IFN-β to suppress viral replication suggests that it might limit virus-induced exacerbations by shortening the duration of the inflammatory response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Anti-Inflammatory Agents / immunology
  • Anti-Inflammatory Agents / pharmacology*
  • Antiviral Agents / immunology
  • Antiviral Agents / pharmacology*
  • Asthma / immunology*
  • Asthma / physiopathology
  • Asthma / virology
  • Bronchi / cytology
  • Bronchi / drug effects*
  • Bronchi / immunology
  • Bronchi / virology
  • Cells, Cultured
  • Epithelial Cells / drug effects*
  • Epithelial Cells / immunology
  • Epithelial Cells / virology
  • Humans
  • Interferon-beta / immunology
  • Interferon-beta / pharmacology*
  • Middle Aged
  • Picornaviridae Infections / immunology
  • Picornaviridae Infections / virology
  • Rhinovirus / drug effects
  • Rhinovirus / immunology
  • Rhinovirus / pathogenicity*
  • Young Adult


  • Anti-Inflammatory Agents
  • Antiviral Agents
  • Interferon-beta