牙龈卟啉单胞菌对牙龈上皮细胞焦点黏附成分paxillin和FAK的作用  

Effects of Porphyromonas gingivalis on focal adhesive components paxillin and FAK of gingival epithelial cells

作　　者：寇育荣[1] 潘亚萍[1] 

机构地区：[1]沈阳市中国医科大学口腔医学院口腔内科,110002

出　　处：《实用口腔医学杂志》2010年第1期10-14,共5页Journal of Practical Stomatology

基　　金：辽宁省教育厅科学技术研究项目(编号:20060993)

摘　　要：目的:研究牙龈卟啉单胞菌(P.gingivalis)对牙周组织的破坏机制,探讨菌毛的致病作用。方法:应用Western blot法检测P.gingivalis ATCC 33277及其fimA缺陷突变株对Hela细胞及永生化人牙龈上皮细胞(immortalized human gingival epi-thelial cells,IHGE细胞)的焦点黏附成分——焦点黏附蛋白paxillin和焦点黏附激酶(focal adhesion kinase,FAK)蛋白表达的影响。结果:P.gingivalis ATCC 33277野生株和fimA缺陷突变株能够使HeLa细胞和IHGE细胞的paxillin和FAK发生降解,fimA缺陷突变株对paxillin和FAK的降解能力较野生株显著减弱。在IHGE细胞中,paxillin和FAK的降解呈时间依赖性和MOI依赖性。结论:菌毛介导的P.gingivalis的黏附和侵入可能对焦点黏附成分的降解起促进作用,IHGE细胞较Hela细胞更适用于牙周致病菌的研究。Objectives：To explore the destructive mechanism of P.gingivalis on periodontium and to better understand the pathogenic effects of P.gingivalis fimbriae.Methods：Western blotting was used to detect the degradation effects of P.gingivalis ATCC 33277 and its fimA-deficient mutant on focal adhesion components paxillin and focal adhesion kinase（FAK） of Hela cells and immortalized gingival epithelial cells（IHGE cells）.Results：P.gingivalis ATCC 33277 wild strain and its fimA-deficient mutant induced degradation of paxillin and FAK both in Hela cells and in IHGE cells.fimA-deficient mutant had a remarkable weaker degradation ability than the wild strain.In IHGE cells,paxillin and FAK were degraded in a time-and MOI-dependent manner.Conclusion：P.gingivalis fimbriae-mediated adhesion and invasion to epithelial cells may promote the degradation of focal adhesion components.IHGE cells may be more suitable for the study of periodontal pathogens than Hela cells.

关 键 词：牙龈卟啉单胞菌 桩蛋白 焦点黏附激酶 

分 类 号：R78[医药卫生—口腔医学]