布地奈德对哮喘小鼠模型IL-22的调控作用

目的观察白介素22(IL-22)在哮喘模型中的作用,研究布地奈德对哮喘小鼠模型气道炎症及IL-22的调控作用。方法 24只BALB/c小鼠随机分为对照组、哮喘模型组和布地奈德组3组,用卵清蛋白(OVA)致敏、激发小鼠以制备哮喘模型。小鼠肺组织进行HE及AB-PAS染色,进行气道炎症评分,ELISA法检测3组小鼠肺泡灌洗液(BALF)中IL-22的水平,实时荧光定量PCR检测小鼠肺组织中IL-22mRNA的表达水平。结果与对照组相比较,哮喘小鼠肺组织炎症评分增加,BALF中IL-22水平增高,肺组织中IL-22mRNA表达水平升高,差异均具有统计学意义。给予布地奈德治疗后,小鼠气道炎症评分及肺组织IL-22mRNA的表达水平均较哮喘组降低,差异具有统计学意义。结论布地奈德对哮喘气道炎症的治疗作用与其抑制肺内IL-22的表达和分泌有关。

Budesonide inhibits murine asthmatic airway inflammation through reduction IL-22 secretion

Objective To study the effect of Interleukin-22 (IL-22) on murine asthmatic airway inflammation and airway remodeling, observe the effect of budesonide on IL-22 of asthmatic mouse model, explore the mechanism of budesonide in the treatment of asthma. Methods Ovalbumin(OVA) was used as an allergen to sensitize and challenge the mice. 24 female specific-free (SPF) BALB/c mice aged four weeks were randomly divided into 3 groups:control group, asthma group and budesonide treatment group (BUD group). For Histopathological Examination, HE staining was used to measure the inflammation scores, AB-PAS staining was used to measure the hyperplasia of goblet cells and mucin. Enzyme-linked immunosorbent assay(ELISA) was used to analyze IL-22 levels in bronchoalveolar lavage fluid (BALF). Quantitative Real-time PCR was performed to analyze the effects of budesonide on IL-22 mRNA levels in lung tissue. Results The inflammation scores of asthma group were elevated compared with the control group. An overall change towards less severe asthmatic airway inflammation by the end of the trial was observed in the BUD group. IL-22 levels in BALF were significant decreased after the treatment of budesonide, the mRNA levels of IL-22 were obviously decreased in BUD group, too. A significant positive correlation was observed between the mRNA levels of IL-22 and airway inflammation. Conclusions The increasing IL-22 secretion can lead to the occurrence of airway inflammation of asthma. Budesonide can inhibit the expression of IL-22, thereby Budesonide could inhibit the development of airway inflammation of asthma.