CAJ | 학술논문

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 epithelial 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.
목적:연구아간계람단포균(P.gingivalis)대아주조직적파배궤제,탐토균모적치병작용.방법:응용Western blot법검측P.gingivalis ATCC 33277급기fimA결함돌변주대Hela세포급영생화인아간상피세포 (immortalized human gingival epithelial cells, IHGE세포) 적초점점부성분——초점점부단백paxillin화초점점부격매 (focal adhesion kinase,FAK) 단백표체적영향.결과:P.gingivalis ATCC 33277야생주화fimA결함돌변주능구사HeLa세포화IHGE세포적paxillin화FAK발생강해,fimA결함돌변주대paxillin화FAK적강해능력교야생주현저감약.재IHGE세포중,paxillin화FAK적강해정시간의뢰성화MOI의뢰성.결론:균모개도적P.gingivalis적점부화침입가능대초점점부성분적강해기촉진작용,IHGE세포교Hela세포경괄용우아주치병균적연구.
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.