摘要
目的探讨脾虚证易并发白色念珠菌感染的免疫学机制,为临床防治白色念珠菌感染和脾虚证提供依据。方法将40只昆明小鼠分层随机分成4组,即正常对照组(A组)、脾虚模型组(B组)、正常感染白色念珠菌组(C组)、脾虚感染白色念珠菌组(D组)。采用饮食失节加劳倦过度的复合因素制备小鼠脾虚证模型。模型成功后,经口灌给C、D组小鼠白色念珠菌悬液,A、B组给予生理盐水。3周后,应用动物血液分析仪检测小鼠外周血细胞数量,应用酶联免疫吸附法测定腹腔巨噬细胞及血清中白细胞介素-1β(IL-1β)的表达水平。结果脾虚小鼠感染白色念珠菌后期,单核细胞数明显升高(P<0.01),中性粒细胞也明显增加;腹腔巨噬细胞及血清中IL-1β表达水平明显高于其他各组(P<0.01)。结论脾虚小鼠对消化道感染白色念珠菌的易感性增强,感染后期体内表达炎性细胞因子IL-1β的水平明显增高。
Objective To investigate the immunological mechanism of Candida albicans infection in the state of spleen deficiency,and provide basis for the prevention and treatment of the infection.Methods Forty KM mice were randomly divided into four groups:the normal control group(A group),spleen deficiency model group(B group),Candida albicans infection in normal group(C group),spleen deficiency with Candida albicans infection group(D group).The animal model of spleen deficiency was prepared by irregular-feeding and overstrain methods.The mice in group C and D were fed with suspension of Candida albicans,and group A and B were fed with NS.After 3 weeks,the number of peripheral blood cells were measured with animal blood analyzer,the expression of interleukin-1β(IL-1β) of peritoneal macrophages and serum were detected by enzyme-linked immunosorbent assay(ELISA).Results The number of mononuclear cells increased significantly in spleen deficiency mice in the final infectious stage(P0.01),and neutrophils also significantly increased.The expression of IL-1β of peritoneal macrophages and serum of group D was significantly higher than the other groups(P0.01).Conclusion The susceptibility of alimentary tract infection of Candida Albicans was increased under the condition of spleen deficiency,and the expression of inflammatory cytokine IL-1β was significantly increased in the final infectious stage.
出处
《中国中医药信息杂志》
CAS
CSCD
2011年第11期41-43,共3页
Chinese Journal of Information on Traditional Chinese Medicine
基金
国家中医药管理局资助项目(06-07JP13)
辽宁省教育厅博士生访学项目(辽教发[2008]16号)
关键词
白色念珠菌
脾虚证
感染
细胞因子
小鼠
Candida Albicans
spleen deficiency syndrome
infection
cytokine
mice