title: Impaired virus-induced interferon-alpha2 release in adult asthmatic patients.
abstract: 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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Experimental Pneumology, Ruhr-University Bochum, Bochum, Germany. kirsten.gehlhar@rub.de
authors.forename: K
authors.initials: K
authors.lastname: Gehlhar
authors.forename: C
authors.initials: C
authors.lastname: Bilitewski
authors.forename: K
authors.initials: K
authors.lastname: Reinitz-Rademacher
authors.forename: G
authors.initials: G
authors.lastname: Rohde
authors.forename: A
authors.initials: A
authors.lastname: Bufe
mesh_terms: D000328:Adult; D001249:Asthma / Q000276:immunology*; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D007108:Immune Tolerance; D016898:Interferon-alpha / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009522:Newcastle disease virus / Q000276:immunology*; D011446:Prospective Studies; D012333:RNA, Messenger / Q000235:genetics; D012136:Respiratory Syncytial Viruses / Q000276:immunology*; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D014158:Transcription, Genetic
chemical_list: D016898:Interferon-alpha; D012333:RNA, Messenger