高脂血症抑制载脂蛋白E基因敲除小鼠对牙龈卟啉单胞菌炎症反应的影响  

Hyperlipidemia inhibited inflammatory response to Porphyromonas gingivalis in apolipoprotein E knockout mice

作　　者：雷浪[1] 李厚轩[1] 黄美香[1] 陈帅[1] 闫福华[2] 

机构地区：[1]福建医科大学附属口腔医院.口腔医学院,福建福州350002 [2]南京大学医学院附属口腔医院,江苏南京210008

出　　处：《上海口腔医学》2014年第4期409-412,共4页Shanghai Journal of Stomatology

基　　金：国家自然科学基金(81170973;81100760)~~

摘　　要：目的:研究高脂血症在ApoE基因敲除(ApoE-/-)小鼠对牙龈卟啉单胞菌(P.gingivalis)炎症反应过程中的影响及其机制。方法:利用ApoE-/-小鼠建立长时间高脂血症模型,腹腔注射活P.gingivalis以建立腹膜炎症模型,倍比稀释法分析腹腔内清除细菌能力,ELISA法检测血液中白细胞介素6(IL-6)和单核细胞趋化因子1(MCP-1)的分泌,实时定量PCR检测腹腔细胞IL-6和MCP-1的转录水平,采用SPSS13.0软件包进行统计学分析。结果:高脂血症显著降低了腹腔清除P.gingivalis的能力,ApoE-/-小鼠腹腔细胞中IL-6和MCP-1转录水平下降,释放入血液中的IL-6和MCP-1水平下降。结论:高脂血症导致宿主对P.gingivalis炎症反应不足,清除细菌能力下降,加速了牙周病的发展进程。PURPOSE： To investigate the effect and mechanism of hyperlipidemia on inflammatory response to Porphyromonas gingivalis （19. gingivalis） in apolipoprotein E knock out （ApoE -/-） mice. METHODS： Long term hyperlipidemia model was established in ApoE-/- mice, and viable P. gingivalis were injected into peritoneal cavity to make peritonitis model. Bacteria clearance capability was detected by serial dilution, production of pro-inflammatory cytokine interleukin-6 （IL-6） and monocyte ehemotactic protein-1 （MCP-1）in serum was measured by ELISA, and IL-6 as well as MCP-1 transcription in peritoneal cells was determined by real time PCR. The data was analyzed with SPSS13.0 software package. RESULTS： Hyperlipidemia disrupted P. gingivalis clearance capability in ApoE-/- mice, accompanied by inhibited IL-6 and MCP-1 transcription in peritoneal ceils and decreased IL-6 and MCP-1 release into blood. CONCLUSIONS： Hyperlipidemia disrupts inflammatory response to P. gingivalis, leading to decreased bacteria clearance, which may affect periodontitis progression.

关 键 词：高脂血症 牙龈卟啉单胞菌 牙周病 

分 类 号：R781.4[医药卫生—口腔医学]