The Role Of Interleukin 13 Receptor Alpha 2 In Airway Remodeling Of Bronchial Asthma

PartⅠMice Model of AsthmaPurpose: To build stable and reproductive model of asthmatic mices.Methods: Male mices (n=24) were randomly divided into a control group(n=8), an asthmatic group(n=8) and a dexamethasone group(n=8). Asthmatic model was established. Airway responsiveness was measured and the change of airway histology was observed.Results: (1) Expiration resistance was determined before and after injection of acetylcholine chloride(5～405μg/μl), and expiration resistances of the asthmatic group were significantly elevated compared with those of the control group(P＜0.01); expiration resistances of the dexamethasone group were significantly reduced compared with those of the asthmatic group(P＜0.05). (2) In the asthmatic group, the thicknesses of WAt/Pi and WAm/Pi were all significantly higher than those of the control group(P＜0.01); In the dexamethasone group, the thicknesses of WAt/Pi and WAm/Pi all were significantly lower than those of the asthmatic group(P＜0.01).Conclusions: Asthmatic mices were successfully established and could be used in further study. PartⅡThe Expression and the Role of Interleukin 13 Receptor alpha 2 in Airway Remodeling of Bronchial AsthmaObjective: To investigate the expression of IL-13Ra2 in bronchioles of asthmatic mice,and to observe the relationship between the expression of IL-13Rα2 and airway remodeling.Methods: Asthmatic model of mice was established. Thirty-two male BALB/c mices were randomly divided into a control group, an asthmatic group, a dexamethasone group, and an Interferon-γgroup. The change of airway histology was observed. The expression of IL-13Rα2 in lung tissues were determined by immunohistochemical staining and photographic analysis. The rnRNA expressions of IL-13Rα2,c-Fos and TGF-β1 in the lungs were detected by reverse transcription-polymerase chain reaction(RT-PCR).Results: (1).In the asthmatic group, the numbers of eosinophils and lymphocytes, the thicknesses of Wat/Pi and Wam/Pi were all significantly higher than those of the control group(P＜0.01); In the dexamethasone group and Interferon-γgroup, the numbers of eosinophils and lymphocytes, the thicknesses of Wat/Pi and Wam/Pi all were significantly lower than those of the asthmatic group(P＜0.01). (2).In the asthmatic group, the mRNA expressions of IL-13Rα2, c-jun and TGF-β1 were significantly increased compared with those of the control group(P＜0.01), In dexamethasone group, the expressions of IL-13Rα2, c-Fos and TGF-β1 mRNA were all low; In the Interferon-y group, the expressions of TGF-β1 mRNA were decreased compared with those of the asthmatic group(P＜0.01), but the mRNA expression of IL-13Rα2 and c-Fos was no significantly change compared with those of the asthma group(P＞0.05); (3).In asthma group, the expression of IL-13Rα2 protein by immunohistochemical staining was significantly increased compared with those of the control group(P＜0.01), in dexamethasone group and the Interferon-γgroup, the expressions of IL-13Rα2 protein were decreased compared with those of the asthmatic group(P＜0.01).Conclusions: The expression of IL-13Rα2 in bronchioles of asthmatic mice was increased, the administration of Interferon-γrelieved the severity of airway remodelin, the mechanism was down-regulation of IL-13Rα2 protein expression in response to IFN-γ.