| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1995: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Research Abstract |
Pro-inflammatory cytokines, such as LI-1 beta, TNF-alpha, and IFN-r, suppress HBV replication. The precise mechanism of anti-HBV effect by these cytokines is not clarified. We examined the anti-HBV effect of pro-inflammatory cytokines in relation with NF-kappa B.Materials and Method : 3HB-neo, in which tandemly arranged HBV genomes were transfected, can produce HBVDNA into cultured media. Various concentrations of LI-1 beta, TNF-alpha, and IFN-r were added into the cultured media. The degree of HBV replication was judged by HBVDNA in the media and mRNA within cells. NF-kappa B activity was examined by gel-shift assay. Results ; LI-1 beta (0,4,20,100U/ml), TNF-alpha (0,10,50,250U/ml), and IFN-r (0,10,50,250U/ml) suppressed HBV replication in a dose-dependent manner at 24 hrs after addition. HBVmRNA in 3HB-neo showed the same way as HBV in the media. Li-1 beta, TNF-alpha, and IFN-r activate NF-kappa B.Furthermore, 30mM NAC,an inhibitor of NF-kappa B,blocked the anti-HBV effect by pro-inflammatory cytokines. Conclusion : We find a consensus sequence of NF-kappa B on the HBV genome (adr). Since Anti-HBV effect by LI-1 beta, TNF-alpha, and IFN-r coincides with the increased activation of NF-kappa B,we speculate that NF-kappa B may work as a negative regulator of HBV replication within cells.
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