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.
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.