| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2003: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2002: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Research Abstract |
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.
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