摘要
目的了解早期气道接触细菌抗原对辅助性T淋巴细胞1/2(Th1/Th2)平衡以及大鼠成年后哮喘气道炎症的影响,研究哮喘的发病机制。方法将新生SD大鼠随机分为3个细菌抗原组、哮喘组及对照组,细菌抗原组大鼠分别于出生后第1、3、5、7 d鼻咽部给予107、106、105灭活肺炎链球菌10μL,哮喘组及对照组大鼠则给予磷酸盐缓冲液(PBS)10μL;大鼠饲养至成年后造模,观察各组大鼠肺组织病理、支气管肺泡灌洗液(BALF)白细胞分类、血清中白细胞介素-4(IL-4)、γ-干扰素(IFN-γ)、卵蛋白-IgE含量。结果肺组织病理显示,早期接触灭活细菌的大鼠气道炎症较重;107、106抗原组大鼠BALF中淋巴细胞百分比为(32.94±13.62)%、(29.50±8.92)%,与哮喘组比较明显增多(P<0.05);107抗原组大鼠血清中卵蛋白-IgE水平(0.33±0.07)较哮喘组明显升高(P<0.01),IFN-γ水平为(11.93±2.74)pg/mL,较哮喘组明显下降(P<0.05)。结论早期气道接触细菌抗原可加重Th1/Th2失衡以及大鼠成年后哮喘气道炎症。
Objective To investigate the effect of early exposure of airway to bacterial allergen on the balance of T-helper-1 cells/T-helper-2 cells(Th1/Th2) and the asthmatic airway inflammation of adult rats and to understand the pathogenic mechanism of asthma.Methods New born rats were randomly divided into bacterial allergen exposure group,asthma group and control group.The rats of bacterial allergen exposure group were given 10 μL inactivated Streptococcus pneumoniae via nose drip at 1,3,5 and 7 days after the birth.The asthma group and control group were given 10 μL phosphate buffer solution(PBS) instead.When all rats were kept to adulthood the asthmatic model was made.The pathologic changes of lung tissue,differentiation of bronchoalveolar lavage fluid and serum interleukin-4(IL-4),interferon-γ(IFN-γ) and ovalbumin-specific IgE were observed.Results The airway inflammation in all allergen exposure groups were severe.The ratio of lymphocyte of 107 and 106 allergen exposure groups were 32.94±13.62% and 29.50±8.92%,and were increased significantly compared with those of asthma group(P0.05).The serum ovalbumin-specific IgE of 107 allergen exposure group(0.33±0.07)was increased significantly(P0.01).While the interferon gamma(IFN-γ)(11.93±2.74 pg/mL) was significantly decreased(P0.05).Conclusion Early exposure of the airway to bacterial allergen could aggravate the imbalance of Th1/Th2 and asthmatic airway inflammation in adult rats.
出处
《中国公共卫生》
CAS
CSCD
北大核心
2011年第6期751-752,共2页
Chinese Journal of Public Health
关键词
大鼠
哮喘
细菌抗原
气道炎症
卵蛋白
rat
asthma
bacterial allergen
airway inflammation
ovalbumin