牙龈卟啉单胞菌感染对牙龈上皮细胞中基质金属蛋白酶13表达的影响

 目的 通过体外建立牙龈卟啉单胞菌（P. gingivalis）感染牙龈上皮细胞模型，探讨P. gingivalis W83、ATCC 33277感染牙龈上皮细胞后基质金属蛋白酶13（MMP-13）表达的变化。方法 将P. gingivalis W83、ATCC 33277作用于牙龈上皮细胞6、12、24和48 h，采用ELISA检测上清液中MMP-13蛋白浓度变化，实时PCR 检测MMP-13 mRNA相对含量变化。结果 P. gingivalis感染牙龈上皮细胞后，MMP-13蛋白和mRNA表达的总体趋势随时间的延长表达水平逐渐增高。P. gingivalis感染牙龈上皮细胞6和12 h后， P. gingivalis ATCC 33277感染组和W83感染组MMP-13蛋白表达水平与对照组相比无明显差异，而MMP-13 mRNA的相对表达量高于对照组（P＜0.05）；感染24和48 h后，P. gingivalis ATCC 33277感染组和W83感染组MMP-13蛋白和mRNA的相对表达量均明显高于对照组（P＜0.05），且P. gingivalis W83感染组MMP-13明显高于P. gingivalis ATCC 33277感染组（P＜0.05）。结论 P. gingivalis能够促进牙龈上皮细胞分泌MMP-13，造成牙周组织破坏。P. gingivalis W83降解细胞外基质的能力高于P. gingivalis ATCC 33277，更利于细菌向深部组织扩散。

Effect of Porphyromonas Gingivalis on the Expression of MMP-13 in Human Gingival Epithelial Cells

Objective To investigate the effects of Porphyromonas gingivalis(P.gingivalis)on the expression of matrix metal proteinase13(MMP-13)in immortal human gingival epithelial cells(IHGECs)using an in vitro model.Methods The protein level and mRNA relative expression of MMP-13 were determined by ELISA and real-time RT-PCR at different time intervals(6 h,12 h,24 h,and 48 h)following continuous co-culture of P.gingivalis W83 and ATCC33277 with IHGECs.Results The protein level and mRNA relative expression of MMP-13 were increased in IHGECs infected with P.gingivalis.When IHGECs were treated with P.gingivalis at 6 h after infection,the MMP-13 protein expression in the experimental and control groups showed no obvious difference,but the MMP-13 mRNA relative amount was higher in experimental group than in the control group.When IHGECs were treated with P.gingivalis from 24 h to 48 h after infection, the protein and mRNA expressions of MMP-13 in experimental groups were significantly higher than those in the control group.The MMP-13 secretion stimulated by P.gingivalis W83 was significantly higher than that by P.gingivalis 33277.Conclusion P.gingivalis accelerates secretion of MMP-13 in IHGECs,which causes periodontal tissue destruction.P.gingivalis W83 has stronger pathogenicity for periodontal diseases by producing extracellular matrix.