Nakane A, Okamoto M, Asano M, Kohanawa M, Satoh Y, Minagawa T
Department of Microbiology, Hokkaido University School of Medicine, Sapporo, Japan.
FEMS Immunol Med Microbiol. 1994 Aug;9(2):163-70. doi: 10.1111/j.1574-695X.1994.tb00487.x.
The effects of dexamethasone (DEX) on a lethal infection with Listeria monocytogenes were studied in mice. Mice were completely protected against the lethal infection when treated with 3.3 mg per kg of DEX. The effect was observed only when DEX was injected before infection. The control mice died from day 3 to day 5 of infection, whereas DEX-treated mice could eliminate L. monocytogenes cells from the organs by day 11 of infection. High titres of endogenous tumour necrosis factor (TNF), interleukin-6 (IL-6) and gamma interferon (IFN-gamma) were induced in the bloodstreams and organs of the drug-free mice. DEX suppressed IL-6 production, but augmented TNF and IFN-gamma production within 24 h of infection, whereas production of all three endogenous cytokines was suppressed in the DEX-treated mice on day 3 of infection when the control mice began to die. These results suggest that DEX shows a protective effect on a lethal infection with L. monocytogenes in mice and that regulation of production of endogenous cytokines might be involved in the effect of DEX.
研究了地塞米松（DEX）对小鼠单核细胞增生李斯特菌致死性感染的影响。当以每千克3.3毫克的剂量给小鼠注射DEX时，小鼠完全受到保护，免受致死性感染。仅在感染前注射DEX时才观察到这种效果。对照小鼠在感染的第3天至第5天死亡，而接受DEX治疗的小鼠在感染第11天时能够从器官中清除单核细胞增生李斯特菌细胞。在未用药小鼠的血液和器官中诱导产生了高滴度的内源性肿瘤坏死因子（TNF）、白细胞介素-6（IL-6）和γ干扰素（IFN-γ）。DEX抑制IL-6的产生，但在感染后24小时内增强TNF和IFN-γ的产生，而在感染第3天对照小鼠开始死亡时，接受DEX治疗的小鼠体内所有三种内源性细胞因子的产生均受到抑制。这些结果表明，DEX对小鼠单核细胞增生李斯特菌致死性感染具有保护作用，内源性细胞因子产生的调节可能与DEX的这种作用有关。
