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

牙周病致病菌牙龈卟啉单胞菌的入侵能够诱导炎症细胞因子的表达。

基本信息

批准号：
14571748
负责人：
TAKESHITA Akira
金额：
$ 1.79万
依托单位：
Meikai University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2002
资助国家：
日本
起止时间：
2002 至 2003
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14571748/
关键词：
P.gingivalis IL-6 Periodontal disease Oral epithelial cell Cytokine Invasion Osteoblast ODF RANKL P. gingivalis 上皮細胞内侵入 invasion 炎症

项目摘要

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.

大牙龈卟啉单胞菌（P.gingivalis） (41kDa)-菌毛抗血清预处理可明显抑制牙龈卟啉单胞菌对人上皮细胞系KB细胞的粘附和侵袭。在这项研究中，我们发现细菌矿工(67kDa)-菌毛的抗血清完全阻断了细菌的入侵，但不能阻止其粘附。另一方面，我们观察到牙龈菌能够刺激KB细胞中IL-6基因的表达。这种刺激作用可通过预处理抗4lkda -菌毛抗血清消除，但菌毛不能刺激IL-6基因表达。有趣的是，我们观察到这种细胞因子的刺激被67kda -菌毛的抗血清预处理完全抑制。此外，在抗菌保护实验（侵袭实验）条件下观察到刺激作用。此外，侵袭抑制剂如MDC、瓦巴因、秋水仙碱、诺可唑和细胞chalacine d预处理可显著抑制牙龈假单胞菌刺激的细胞因子表达。我们认为牙龈假单胞菌的侵袭是由两种类型的菌毛联合介导的，并可能通过表达炎症细胞因子在牙周病中发挥毒力机制。我观察到MAP激酶p38抑制剂SB202190能够完全阻断细胞中细菌诱导的il -6。因此，牙龈假单胞菌侵袭可通过激活细胞中的p38诱导IL-6基因表达。此外，我观察到细菌诱导ODF/RANKL在成骨细胞系MC3T3-E1细胞中的原表达。