摘要
目的:研究卡氏肺孢子菌(Pneumocystis carinii,Pc)肺炎鼠肺Dectin-1、TLR-2和TLR-4的表达,探讨模式识别受体表达改变与PCP疾病发生的相互关系。方法实验分4组:正常对照组、Pc刺激组、PCP模型组以及PCP模型恢复组。地塞米松磷酸钠免疫抑制方法建立PCP动物模型,改良四胺银(GMS)染色检测Pc包囊;肺组织切片HE染色观察肺组织病理变化;实时荧光定量和Western-blot检测Dectin-1、TLR-2和TLR-4的mRNA以及蛋白的表达。结果:Pc刺激组的Dectin-1、TLR-2以及TLR-4的mRNA以及蛋白的表达明显高于正常对照组(P<0.05);Pc刺激组和PCP恢复组Dectin-1的mRNA以及蛋白显著高于PCP组(P<0.05),而肺部Pc载荷量显著低于PCP组(P<0.05)。结论地塞米松抑制了PCP鼠肺Dectin-1、TLR-2和TLR-4受体的表达,这可能与PCP疾病的发生和发展有关。
Objective： To study the expression of Dectin - 1 ,TLR - 2 and TLR-4-in Pneumocystis carinii pneumonia （PCP） rat, and to explore the influence of dexamethasone on the expression of Dectin - 1 ,TLR- 2 and TLR - 4 and its relationship with progression of PCP. Methods Rat were divided into four groups which were normal control, treated with P. carinii {Pc）, PCP model and recovered PCP model. PCP rat were induced with dexamethasone in this study, and Pc cysts were detected by GMS stains. Real - time PCR and Western blot were utilized to detected the expression of Dectin - 1, TLR - 2 and TLR - 4 in lung. Results The expression of Dectin- 1,TLR- 2 and TLR-4 were much higher in the treated group with Pc than that of the normal group（ P 〈0.05}. The expression of Dectin - 1 were much higher in the treated group and recovered PCP group than that of PCP model group{P 〈 0.05）, while the burden of Pccysts was just the reverse（P〈 0.05）. Conclusion Dexamethasone inhibited the expression of Dectin- 1 ,TLR- 2 and TLR-4 in lung of rat , which may be one of mechanisms of PCP development induced by P. carinii. Key words： Pneumocvstis carinii ; dectin - 1, TLR - 2; TLR - 4 ; rat modle
出处
《激光杂志》
CAS
CSCD
北大核心
2013年第6期110-112,共3页
Laser Journal
基金
中国国家自然科学青年基金(81000745)
重庆市卫生局医学科学项目(2009)66,(2010)51.
