李斯特菌感染期间白细胞介素-6、肿瘤坏死因子和白细胞介素-1的相互作用。
Interaction of interleukin-6, tumour necrosis factor and interleukin-1 during Listeria infection.
作者信息
Liu Z, Simpson R J, Cheers C
机构信息
Department of Microbiology, University of Melbourne, Victoria, Australia.
出版信息
Immunology. 1995 Aug;85(4):562-7.
Abstract
Injected recombinant interleukin-6 (IL-6), tumour necrosis factor (TNF) and IL-1 all protect mice against experimental infection with Listeria monocytogenes. We have therefore investigated the interaction of these cytokines during infection. Treatment with recombinant (r)IL-6 enhanced TNF production by spleen cells during the first 2 days of infection. Anti-TNF antibody could totally abolish the protective effect of rIL-6, while the optimal protective function of TNF could not be achieved when IL-6 was neutralized by anti-IL-6 antibody. IL-1 induced a high level of IL-6 in the serum a short time after its administration, and neutralization of IL-6 totally abolished the protective function of rIL-1. The results thus provide further evidence for the complexity of cytokine interaction.
摘要
注射重组白细胞介素-6（IL-6）、肿瘤坏死因子（TNF）和IL-1均可保护小鼠抵御单核细胞增生李斯特菌的实验性感染。因此，我们研究了这些细胞因子在感染过程中的相互作用。在感染的头两天，用重组（r）IL-6处理可增强脾细胞产生TNF。抗TNF抗体可完全消除rIL-6的保护作用，而当IL-6被抗IL-6抗体中和时，TNF的最佳保护功能无法实现。IL-1给药后短时间内可诱导血清中高水平的IL-6，而IL-6的中和可完全消除rIL-1的保护功能。这些结果进一步证明了细胞因子相互作用的复杂性。
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本文引用的文献
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