为探讨白细胞介素(interleukin，IL)-33在呼吸道合胞病毒(respiratory syncytial virus，RSV)感染导致哮喘急性加重过程中的作用，选取3周龄雌性BALB/c小鼠28只，随机分为5组，分别为正常对照组、单纯RSV感染组、哮喘组、RSV感染哮喘并对照抗体组、RSV感染哮喘并IL-33抗体治疗组。建立RSV感染的小鼠模型，给予IL-33抗体治疗，并分别取各组小鼠的肺组织行苏木精-伊红染色法 ( hematoxylin-eosin staining，HE )染色；实时反转录聚合酶链反应(real-time reverse transcriptional polymerase chain reaction，real-time RT PCR)检测肺组织中il-13, il-4, 视黄酸受体相关孤儿受体(retinoic acid receptor-related orphan receptor，ror)-γt, 叉头状转录因子3(forkhead box P3，foxp3), 干扰素(interferon，ifn)γ 以及il-33 mRNA表达量；酶联免疫吸附试验(enzyme linked immunosorbent assay，ELISA)检测肺泡灌洗液中IL-13、IL-4、IL-33、IFNγ和IL-17的表达。结果显示RSV感染导致的哮喘急性加重组小鼠气道周围炎性细胞浸润最为明显，且IL-33和T辅助细胞2型(T helper 2, Th2)的主要效应因子IL-4的基因转录和蛋白表达水平明显升高。阻断IL-33后肺组织内炎性细胞浸润减轻，伴随着il-13, il-4, rorγt 和 foxp3的基因转录水平的降低及肺泡灌洗液中IL-4、IL-13、IL-17蛋白表达的减少，但阻断IL-33对IFN-γ的表达无明显影响。结果提示IL-33在RSV感染诱导的哮喘急性发作过程中起致病作用，阻断IL-33可减轻肺部病理变化及炎性因子分泌，可为支气管哮喘急性加重的治疗提供新的靶点。

To study the role of interleukin-33 (IL-33) in acute exacerbation of allergic asthma induced by respiratory syncytial virus (RSV). Female BALB/c mice aged 3 weeks were randomly divided into five groups: PBS control; RSV infection; asthma mice model (sensitized and challenged by 1% ovalbumin); asthma model with RSV infection and treated with control antibody; asthma model with RSV infection and treated with anti-IL-33 antibody. Lung specimens were collected. The Lung sections were stained by hematoxylin-eosin to observe the changes of lung inflammation. il-13, il-4, rorγt, foxp3, ifnγ and il-33 mRNA expressions in the lung tissue were determined by real-time PCR. IL-13、IL-4、IL-33、IFN-γ and IL-17 level in bronchoalveolar lavage fluid(BALF) were measured by ELISA. Histological examination of lung tissue demonstrated that anti-IL-33 significantly inhibited allergen-induced lung inflammation. Both mRNA and protein level of IL-33 and IL-4 were significantly increased in the RSV asthma group. Treatment with anti-IL-33 significantly reduced the concentrations of IL-4, IL-13 and IL-17 compared with administration of a control antibody. The mRNA expression of il-13, il-4, rorγt, and foxp3 were also decreased. There was no change with IFN-γ expression. Our results demonstrated that anti-IL-33 antibodies can prevent the development of asthma in a mouse model, and blockade of IL-33 could be a new therapeutic strategy for acute exacerbation of allergic asthma.