呼吸道合胞病毒感染诱导BALB/c鼠固有免疫细胞分泌IL-33

Respiratory Syncytial Virus Infection Induced Excretion of IL-33 in Innate Immune Cells in BALB /c mice

IL-33是新发现的细胞因子,在病毒感染所诱发的气道炎症反应中发挥重要作用。研究发现感染呼吸道合胞病毒的BALB/c鼠肺组织内IL-33水平明显升高。但RSV感染后分泌IL-33的免疫细胞类型,尤其是感染早期分泌IL-33的固有免疫细胞类型目前尚不清楚。通过分离培养BALB/c鼠肺泡巨噬细胞及树突状细胞,采用ELISA及实时荧光定量PCR法检测上述固有免疫细胞RSV感染后IL-33分泌水平的变化。结果显示,RSV感染72 h后BALB/c鼠肺泡巨噬细胞IL-33mRNA水平明显升高,而树突状细胞RSV感染24 h后IL-33mRNA水平开始上升,48 h达峰值。研究证实RSV感染诱导BALB/c鼠固有免疫细胞分泌IL-33,进而介导感染后炎症的发生发展。

IL-33 is a newly found cytokine;it plays an important role in virus infection induced airway inflammation reaction. It was found in the study that the level of IL-33 was significantly increased in the lungs of BALB/ c mice in-fected with respiratory syncytial virus（RSV）. However,the immune cell types for IL-33 excretion after RSV infec-tion,especially the cell types of the innate immune cells,remain unknown so far. In this study,by isolating and cul-tivating alveolar macrophages and dendritic cells from BALB/ c mice,the change of IL-33 excretion level in innate im-mune cells after infected with RSV were tested and determined with ELISA and real-time PCR. The results showed that at 72 h after RSV infection,the expression of IL-33 mRNA level in the alveolar macrophages increased signifi-cantly. Meanwhile,the expression of IL-33 mRNA level in dendritic cells began to increase 24 h after the infection, and reached to a peak at 48 h after RSV infection. This study has confirmed that RSV infection induced BALB/ c mice innate immune cells to excrete IL-33,and proceed to medium-leading the occurrence and development of inflammation after the infection.