Nakane A, Numata A, Minagawa T
Department of Microbiology, Hokkaido University School of Medicine, Sapporo, Japan.
Infect Immun. 1992 Feb;60(2):523-8. doi: 10.1128/iai.60.2.523-528.1992.
Mice were infected intravenously with a sublethal dose of Listeria monocytogenes cells and then levels of tumor necrosis factor (TNF), interleukin-6 (IL-6), and gamma interferon (IFN-gamma) in the bloodstreams, spleens, and livers were monitored. The maximum level of TNF was detected at 72 h in the spleens and livers, but TNF was never detected in the bloodstreams. IL-6 appeared in the bloodstreams and spleens and peaked at 48 h. The maximum level of IFN-gamma could be detected in all three specimens, and the highest titer was shown in the spleens. Endogenous TNF production was suppressed by in vivo administration of anti-CD4 monoclonal antibody (MAb) or anti-asialo GM1 antibody but not by anti-CD8 MAb, whereas none of these antibodies suppressed endogenous IL-6 production. Endogenous production of neither IL-6 nor IFN-gamma was inhibited in rabbit anti-recombinant mouse TNF-alpha antibody-treated mice. Similarly, production of TNF and IL-6 did not decrease in anti-mouse IFN-gamma MAb-treated animals, but TNF production was augmented in these animals. These results suggest that the these endogenous cytokines are produced by different mechanisms in L. monocytogenes infection.
给小鼠静脉注射亚致死剂量的单核细胞增生李斯特菌,然后监测其血液、脾脏和肝脏中肿瘤坏死因子(TNF)、白细胞介素-6(IL-6)和γ干扰素(IFN-γ)的水平。在脾脏和肝脏中,TNF的最高水平在72小时时被检测到,但在血液中从未检测到TNF。IL-6出现在血液和脾脏中,并在48小时时达到峰值。在所有三个标本中都能检测到IFN-γ的最高水平,且脾脏中的滴度最高。体内给予抗CD4单克隆抗体(MAb)或抗去唾液酸GM1抗体可抑制内源性TNF的产生,但抗CD8 MAb则不能,而这些抗体均未抑制内源性IL-6的产生。在兔抗重组小鼠TNF-α抗体处理的小鼠中,内源性IL-6和IFN-γ的产生均未受到抑制。同样,在抗小鼠IFN-γ MAb处理的动物中,TNF和IL-6的产生并未减少,但这些动物中TNF的产生有所增加。这些结果表明,在单核细胞增生李斯特菌感染中,这些内源性细胞因子是通过不同机制产生的。