Periodontal disease pathogenic bacterium Porphyromonas gingivalis invasion is able to induce the expression of inflammatory cytokines.

用抗牙龈卟啉单胞菌（P.gingivalis major，41 kDa）菌毛的抗血清预处理，可明显抑制牙龈卟啉单胞菌（P.gingivalis，P. gingivalis）对人口腔上皮细胞株KB细胞的粘附和侵袭。在这项研究中，我们发现，抗血清的细菌矿工（67 kDa）-菌毛完全阻断细菌的入侵，但不粘附。另一方面，我们观察到牙龈卟啉单胞菌能够刺激KB细胞中IL-6基因的表达。这种刺激作用可被抗41 kDa菌毛抗血清所消除，但菌毛不能刺激IL-6基因的表达。有趣的是，我们观察到，这种细胞因子的刺激是完全抑制预处理的抗血清为67 kDa-菌毛。此外，在抗菌保护试验（侵袭试验）条件下观察到刺激作用。此外，侵袭抑制剂如MDC、哇巴因、秋水仙碱、诺考达唑和胞松弛素D可显著抑制牙龈卟啉单胞菌刺激的细胞因子表达。提示牙龈卟啉单胞菌的侵袭是由两种菌毛共同介导的，并可能通过表达炎性细胞因子而发挥致病作用。并观察到MAP激酶p38抑制剂SB 202190能够完全阻断细菌诱导的细胞内IL-6的产生。因此，牙龈卟啉单胞菌侵袭能够通过激活细胞中的p38来诱导IL-6基因表达。此外，我观察到细菌诱导成骨细胞系MC 3 T3-E1细胞中ODF/RANKL基因表达。

Porphyromonas gingivalis (P.gingivalis) adherence and invasion to human epithelial cell line KB cells markedly were eliminated by inhibition of the bacterial adherence through pretreatment of antiserum for P.gingivalis major (41kDa)-fimbriae. In this study, we showed that antiserum for the bacterial miner (67kDa)-fimbriae completely blocked the bacterial invasion but not its adherence. On the other hand, we observed that P.gingivalis is able to stimulate expression of IL-6 gene in KB cells. This stimulatory action was eliminated by pretreatment of anti-4lkDa-fimbriae antiserum, nevertheless, the fimbriae are not able to stimulate IL-6 gene expression. Interestingly, we observed that this cytokine stimulation is completely inhibited by pretreatment of antiserum for 67kDa-fimbriae. In addition, the stimulatory action was observed under condition of antibacterial protection assay (invasion assay). Moreover P.gingivalis-stimulated the cytokine expression is significantly inhibited by pretreatment of invasion inhibitors such as MDC, ouabain, colchicine, nocodazole, and cytochalacine D. We suggest here that P.gingivalis invasion is mediated by combination of two types fimbriae and may function as a virulence mechanizm in periodontal disease through expression of inflammatory cytokine. And I observed that MAP kinase p38 inhibitor SB202190 is able to completely block the bacteria-induced IL-6in the cells. Therefore, P.gingivalis invasion is able to induce IL-6 gene expression through activation of p38 in the cells. Moreover I observed that the bacteria induce the gen expression of ODF/RANKL in osteoblastic cell line MC3T3-E1 cells.