Impaired virus-induced interferon-alpha2 release in adult asthmatic patients

Clin Exp Allergy. 2006 Mar;36(3):331-7. doi: 10.1111/j.1365-2222.2006.02450.x.


Background: Interferon-alpha (IFN-alpha) not only serves as a first defence line of the immune system against viral attacks but also interacts with T-helper type 1 (Th1)/ T-helper type 2 (Th2) regulation and various other cell types like basophils and monocytes, thereby linking innate and acquired immunity. Recently, we demonstrated that children with allergic asthma produced significantly lower amounts of virus-induced IFN-alpha2 compared with healthy children or those with intrinsic asthma.

Objective: In this study, we extend our analysis to examine in a cohort study whether IFN-alpha2 is also reduced in allergic asthma of adults.

Methods: Adults with allergic asthma and healthy controls were prospectively recruited. Blood cultures were stimulated with different viruses (respiratory syncytial virus (RSV), newcastle disease virus (NDV)) and analysed for IFN-alpha2 protein release and gene transcription.

Results: Virus-induced IFN-alpha2 release from blood cells of allergic asthmatic patients was significantly reduced compared with healthy controls, independent of the virus used (NDV(asthma)=221+/-134 pg/mL, NDV(healthy)=555+/-341 pg/mL, P=0.003 and RSV(asthma)=46+/-27 pg/mL, RSV(healthy)=108+/-90 pg/mL, P=0.014). Values=mean+/-standard deviation). It was not influenced by medication, especially cortico-steroids. IFN-alpha2 mRNA expression 5 h after NDV stimulation confirmed the ELISA results and correlated well with release data (r=0.397, P=0.033).

Conclusion: Like children, adults with allergic asthma show impaired virus-induced IFN-alpha2 release in whole blood, indicating a systemic phenomenon in patients with bronchial asthma and atopic phenotype. Impaired virus-induced IFN-alpha release could be a marker of inflammation in chronic allergic asthma.

MeSH terms

  • Adult
  • Asthma / immunology*
  • Cells, Cultured
  • Female
  • Humans
  • Immune Tolerance
  • Interferon-alpha / biosynthesis*
  • Interferon-alpha / blood
  • Interferon-alpha / genetics
  • Male
  • Middle Aged
  • Newcastle disease virus / immunology*
  • Prospective Studies
  • RNA, Messenger / genetics
  • Respiratory Syncytial Viruses / immunology*
  • Reverse Transcriptase Polymerase Chain Reaction / methods
  • Transcription, Genetic


  • Interferon-alpha
  • RNA, Messenger