Objective To observe the immune responses of T helper cells 17 ( Th17) to respiratory syncytial virus ( RSV) infection induced lung inflammation in mice, and explore its roles on the host immune responses to RSV.Methods Female BALB/ c mice aged 3 to 5 weeks were randomly divided into a RSV group ( n=18) and a control group ( n = 12) . The mice were intranasally administrated by a 107.5 50% tissue culture infective dose ( TCID50) of RSV in 0.1 mL of culture medium. Sterile medium ( 0.1 mL/ mouse) was used as control. After infected on 1st , 4th, 8th day, the mice were sacrificed, and specimens from the lungs and lymph nodes were collected. The lung sections were stained by hematoxylin-eosin to observe the changes of lung inflammation after RSV infection. IL-17A, IL-17F and IL-23p19 mRNA expressions in the lung tissue were determined by real-time PCR. The frequencies of Th17 subsets in hilar lymph node were analyzed by flow cytometry. Results On 4th day after RSV infection, a typical lung interstitial inflammation was observed. However, this inflammation was alleviated on 8th day after RSV infection. The viral load in the lung tissue on 4th day after RSV infection were 9.208 ±0.548, which was the highest among all RSV subgroups ( P lt;0.001) . IL-23p19 and IL-17A cytokine expressions in the lung tissue were significantly increased on 4th day and 8th day after RSV infection compared with control groups ( P lt;0.01) , and the peak was on 4th day. However, IL-17F mRNA expression in the lung tissue on different day after RSV infection had no significant difference compared with the control group ( P gt;0.05) . The frequencies of Th17 subsets in hilar lymph node on 4th day and 8th day after RSV infection were ( 0.37 ±0.043) % and ( 0.853 ±0.048) % respectively, which were higher than those in control groups ( P lt;0.05) . The frequencies of Th17 on 8th day after RSV infection were significantly higher than that on 4th day after RSV infection ( P lt; 0.01) . Conclusions The expression of IL-17A in the lung tissue is increased and the level of Th17 cells in hilar lymph nodes is also elevated in the lung infected by RSV, which indicates that Th17 cells might be involved in host antiviral immune.
慢性阻塞性肺疾病( COPD) 是由吸烟诱发, 以气流持续受限为特征, 与CD4 + T 细胞及CD8 + T 细胞密切相关的由炎症及自身免疫反应引起的疾病[ 1] 。CD8 + T 细胞发挥效应及其所受调节的机制是COPD 炎症持续放大且戒烟后也不能缓解的关键, 对其在COPD 炎症中免疫作用及机制的研究有助于突破COPD 抗炎治疗和免疫调节治疗的难点, 对遏制甚至逆转COPD 炎症发展进展过程具有重要意义。Tc17 细胞是近年发现的一种分泌前炎症细胞因子IL-17 的CD8 + T 细胞亚群, 其分泌IL-17、IL-21、 IL-22等细胞因子, 与肺部炎症、哮喘、类风湿性关节炎等炎症免疫性疾病关系密切。在COPD 的肺部炎症中, Tc17 细胞很可能是连接CD4 + T 细胞和CD8 + T 细胞的另一条重要途径, 共同参与COPD 的炎症和免疫方面的机制。
ObjectiveTo investigate the effects of acute and chronic ozone exposure on inflammation,structure and function in murine lung. Methods32 C57/BL6 mice were randomly divided into a single (acute) ozone exposed group,a single air exposed group,a multiple (chronic) ozone exposed group (every three days over 6 weeks),and a multiple air exposed group with 8 mice in each group.The mice were exposed to 2.5 ppm of ozone or air for 3 hours per time and sacrificed 24 hours after the last time of ozone exposure.Lung volume,low attenuation area (LAA) percentage,lung function,cell counts and malondialdehyde (MDA) in bronchoalveolar lavage fluid (BALF),8-hydroxy-2'-deoxyguanosine (8-OHdG) in serum,inflammation scores and mean linear intercept (Lm) in lung section were assessed. ResultsCompared with the single air exposed group,single (acute) ozone exposure led to increases in inflammatory cells in BALF,inflammation scores in the lung tissue,MDA in BALF and 8-OHdG in serum,but had no effect on lung volume,LAA percentage,airflow or Lm.Compared with the single (acute) ozone exposed group,the single air exposed group and the multiple air exposed group,multiple (chronic) ozone exposure increased inflammatory cells in BALF,lung volume,LAA percentage,total lung capacity and lung compliance,mediated airflow obstruction,and also increased lung inflammation socres and Lm. ConclusionAcute ozone exposure induced airway/lung inflammation and oxidative stress,while chronic ozone exposure induced airway/lung inflammation,emphysema and airflow obstruction.