呼吸道合胞病毒感染诱导BALB/c鼠固有免疫细胞分泌IL-33

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。

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

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 infected with respiratory syncytial virus (RSV). However, the immune cell types for IL-33 excretion after RSV infection, especially the cell types of the innate immune cells, remain unknown so far. In this study, by isolating and cultivating alveolar macrophages and dendritic cells from BALB/c mice, the change of IL-33 excretion level in innate immune 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 significantly. 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.