Gehlhar K, Bilitewski C, Reinitz-Rademacher K, Rohde G, Bufe A
Experimental Pneumology, Ruhr-University Bochum, Bochum, Germany.
Clin Exp Allergy. 2006 Mar;36(3):331-7. doi: 10.1111/j.1365-2222.2006.02450.x.
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.
In this study, we extend our analysis to examine in a cohort study whether IFN-alpha2 is also reduced in allergic asthma of adults.
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.
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).
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.
α干扰素（IFN-α）不仅作为免疫系统抵御病毒攻击的第一道防线，还与1型辅助性T细胞（Th1）/2型辅助性T细胞（Th2）调节以及嗜碱性粒细胞和单核细胞等多种其他细胞类型相互作用，从而将先天免疫和后天免疫联系起来。最近，我们证明与健康儿童或特发性哮喘儿童相比，过敏性哮喘儿童产生的病毒诱导型IFN-α2量显著降低。
在本队列研究中，我们扩展分析以检查成人过敏性哮喘中IFN-α2是否也降低。
前瞻性招募患有过敏性哮喘的成人和健康对照。用不同病毒（呼吸道合胞病毒（RSV）、新城疫病毒（NDV））刺激血培养物，并分析IFN-α2蛋白释放和基因转录。
与健康对照相比，过敏性哮喘患者血细胞中病毒诱导的IFN-α2释放显著降低，与所用病毒无关（NDV（哮喘）=221±134 pg/mL，NDV（健康）=555±341 pg/mL，P = 0.003；RSV（哮喘）=46±27 pg/mL，RSV（健康）=108±90 pg/mL，P = 0.014）。数值=平均值±标准差。它不受药物影响，尤其是皮质类固醇。NDV刺激后5小时IFN-α2 mRNA表达证实了ELISA结果，并且与释放数据相关性良好（r = 0.397，P = 0.033）。
与儿童一样，患有过敏性哮喘的成人全血中病毒诱导的IFN-α2释放受损，表明支气管哮喘和特应性表型患者存在全身性现象。病毒诱导的IFN-α释放受损可能是慢性过敏性哮喘炎症的一个标志。
