特异性免疫治疗通过改善Th1/Th2免疫失衡减轻哮喘小鼠肺部炎症OACSTPCD

Objective:To investigate the effect of specific immunotherapy(SIT)on pulmonary inflammation in asthmatic mice and its mechanism.Methods:Mice were randomly divided into control group,model group,SIT group,and dexamethasone group.Asthmatic mouse models were established in model group,SIT group,and dexamethasone group.After the modeling and stimulation stage,SIT group was injected with 1 mg OVA,dexamethasone group was injected with 0.075 mg/mL dexamethasone solution,and other rats were injected with PBS solution of equal volume,and then entered the atomization stage.Airway response was detected by pulmonary function apparatus.The inflammatory cells of alveolar lavage fluid(BALF)were observed by Reiss-Giemsa staining.The cytokines interleukin(IL)-13,IL-4,IL-5,and interferon-γ(IFNγ)in BALF were detected by enzyme-linked immunosorbent assay(ELISA).The morphology of lung tissue was observed by hematoxylin-eosin(H-E)staining.The activity of pulmonary airway epithelial goblet cells was observed by periodic acid-Schiff(PAS)staining.IFNγ and IL-4 in lung tissue were detected by flow cytometry.Results:The airway response of model group was higher than that of control group under 6.25,12.50,25.00 μg/kg and 50.00 μg/kg acetylcholine,and the airway response of SIT group and dexamethasone group were lower than that of model group,but there was no significant difference between SIT group and dexamethasone group.Compared with the control group,the total number of BALF cells,centriocytes(%),eosinophils(%),IL-4,IL-5,IL-13,airway epithelial goblet cells and helper T cells 2(Th2)in the model group were all increased,and IFNγ was decreased.The total number of BALF cells,centriocytes(%),eosinophils(%),IL-4,IL-5,IL-13 and airway epithelial goblet cells were decreased in SIT group,and IFNγ was increased.There was no significant difference between SIT group and dexamethasone group.In the control group,the alveolar and airway structures were organized,the airway walls were thin,and the lumen was not narrow.In the model group,the lung tissue structure was significantly damaged and the airway wall was thicker.The alveolar structure was destroyed,the inflammatory infiltration was obvious,and there was edema around the blood vessels.The inflammatory infiltration of lung tissue was improved,the degree of vascular edema was reduced,and the lumen stenosis was relieved in SIT group and dexamethasone group.Conclusion:SIT can relieve airway hyperplasia in asthmatic mice,inhibit the activity of inflammatory cells and inflammatory factors in the BALF,and improve ventilation by inhibiting the hyperplasia of airway epithelial goblet cells.The mechanism of improvement is related to correcting the helper T cell 1/helper T cell 2 immune imbalance in lung tissue.