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.
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 asthmaticpatients 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.