口服酪酸梭菌减轻哮喘小鼠气道炎症的研究

Inhibitory effect of Clostridium butyrium on the inflammatory response in asthmatic mice

目的探讨酪酸梭菌对哮喘小鼠气道炎症的作用。方法 BALB/c小鼠随机分为对照组、哮喘模型组、酪酸梭菌预防组、酪酸梭菌治疗组。除对照组外,其余各组均采用卵清蛋白腹腔注射致敏和雾化吸入激发,建立小鼠哮喘模型,对照组采用生理盐水替代卵清蛋白。预防组和治疗组分别于第0-14天和第15-28天采用酪酸梭菌溶液进行灌胃。末次激发后24 h检测支气管肺泡灌洗液(BALF)中白细胞总数;制作肺组织病理切片,HE染色后光镜下观察病理变化;酶联免疫吸附法(ELISA)检测BALF中细胞因子IL-4、IL-10、IL-13、INF-γ及血清中IL-10和OVA特异性Ig E及Ig G1水平。结果与哮喘模型组相比,预防组和治疗组小鼠BALF中白细胞总数明显降低(P<0.01),小支气管及伴行血管周围炎症明显减轻,BALF中细胞因子IL-4(P<0.01)及IL-13(P<0.001)的水平显著降低,血清中抗OVA特异性Ig E(P<0.001)及Ig G1(P<0.01)水平也显著降低,血中IL-10的水平升高(P<0.01)。结论口服酪酸梭菌可以减轻哮喘小鼠气道炎症,即酪酸梭菌对于哮喘小鼠具有免疫防治作用。

Objective To investigate the effect of Clostridium butyrium（ C. butyricum） on the airway inflammation in asthma mice.Methods Forty BALB / c mice were randomly assigned into four groups： control group,asthma group,C. butyricum prevention group,and C. butyricum treatment group. BALB / c mouse models of asthma were sensitized by intraperitoneal injection of OVA and challenged with1% OVA via aerosol inhalation,while the mice in control group were given normal saline（ NS） instead of OVA. The mice were given C.butyricum by gavage from day 0 to day 14 of the experiment in prevention group or from day 15 to day 28 in treatment group. The total white blood cell count in the bronchoalveolar lavage fluid（ BALF） was determined under light microscopy and the severity of lung inflammation was evaluated using HE staining at 24 h after the final challenge. The concentrations of IL-4,IL-10,IL-13,INF-γ,and OVAspecific Ig E and Ig G1 were detected by enzyme-linked imunosorbent assay（ ELISA） at 24 h after the final challenge. Results Compared with asthma group,the total white blood cell count,the level of IL-4 and IL-13 in the BALF,and OVA specific Ig E and Ig G1 in the blood were significantly decreased in C. butyricum intervention group（ P 0. 01）,while the level of serum IL-10 increased in intervention group（ P 0. 01）. Conclusion Oral C. butyricum can have preventive and therapeutic effect on the airway inflammation in asthma mice.