Comparison of improvement of two kinds of preventative administration of inter-leukin-27 on airway inflammation and impaired phosphorylation of STAT1 in asthma mice / 中国免疫学杂志

ABSTRACT

Objective:Animal models were set up to explore the best preventative intra-nasal administration of interleukin 27 (IL-27)to diminish allergic airway inflammation of asthma and the related molecular mechanisms. Methods:Ninety-six female C57/6J mice were randomly divided into four groups,a group of the control group,a group of asthma group,and two groups of the prevention group. Based on being sensitizing and challenging with Ovalbumin ( OVA ) in the asthma model, two kinds of IL-27 administration asthma animal models were set up,one of which was low-dose-multiple preventive administration before OVA sensitization,one was low-dose-multiple preventive administration after OVA sensitization but before OVA challenge. Sacrificed the mice after challenging and analyzed the IL-5 and IL-13 levels in supernatant of Broncho alveolar lavage fluid( BAL) using ELISA;and HE stain and inflammation score were done for the lungs. Sacrificed the mice before challenging and used the lungs to analyze the level of total signal transducer and activator of transcription-1(STAT1) protein and phos-STAT1 based on the method of Western blot. Results: In low-dose-multiple administration before sensitization preventions group,IL-27 inhibits the secretion of IL-5 and IL-13(P0. 05 ) . The phosphorylation of STAT1 was impaired in mice after OVA sensitization, and preventative administration of IL-27 before sensitization could reverse the impairment of STAT1, whereas another group had no obviously changes. Conclusion:Preventative administration of IL-27 before sensitization can attenuate the airway inflammation in the mouse asthma model via reversing the phosphorylation of STAT1,while the mice which has been sensitized resisting the inhibition of IL-27 due to the impairment of the phosphorylation of STAT1 and already committed Th2-CD4+T cells existed in sensitization-mice airway might be the reason for such IL-27 resistance.