CAJ | 학술논문

提目的：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。
제목적：연구잡씨폐포자균（Pneumocystis carinii ，Pc）폐염서폐Dectin -1、TLR-2화TLR-4적표체，탐토모식식별수체표체개변여PCP질병발생적상호관계。방법실험분4조：정상대조조、Pc자격조、PCP모형조이급PCP모형회복조。지새미송린산납면역억제방법건립 PCP동물모형，개량사알은（GMS ）염색검측Pc포낭；폐조직절편HE염색관찰폐조직병리변화；실시형광정량화Western -blot검측 Dectin -1、TLR-2화TLR-4적mRNA이급단백적표체。결과：Pc자격조적Dectin -1、TLR-2이급TLR-4적mRNA이급단백적표체명현고우정상대조조（P＜0．05）；Pc자격조화PCP회복조Dectin -1적mRNA이급단백현저고우PCP조（P＜0．05），이폐부Pc재하량현저저우PCP조（P＜0．05）。결론지새미송억제료PCP서폐Dectin -1、TLR-2화TLR-4수체적표체，저가능여PCP질병적발생화발전유관。
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 .