单核细胞增生李斯特菌感染不同阶段小鼠血清中白细胞介素-12、γ干扰素和肿瘤坏死因子α分泌的评价

María A Puertollano, Lidia Cruz-Chamorro, Elena Puertollano, María T Pérez-Toscano, Gerardo Alvarez de Cienfuegos, Manuel A de Pablo
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引用次数: 20

摘要

最近的实验观察已经确定,长链n-3多不饱和脂肪酸抑制免疫功能,并参与降低传染病的抵抗力。BALB/c小鼠在4周内分别饲喂橄榄油、鱼油、氢化椰子油和低脂饮食。用酶联免疫吸附法测定饲喂这些饲料和单核细胞增生李斯特菌攻毒小鼠血清中白细胞介素-12p70 (IL-12p70)、γ干扰素(ifn - γ)和肿瘤坏死因子α (tnf - α)的产生。此外,在感染后24、72和96小时对小鼠脾脏进行细菌计数。在这里,我们量化了IL-12p70和ifn - γ产生的初始减少,这两种物质似乎在降低宿主对单核增生乳杆菌感染的抗性中起重要作用。此外,在感染96小时后,在喂食含有OO的小鼠的脾脏中观察到单核细胞增生乳杆菌的有效消除,尽管IL-12p70和tnf - α的产生减少,这表明免疫抵抗得到改善。总的来说,我们的研究结果表明,单核增生乳杆菌感染前IL-12和ifn - γ产生的初始减少是最相关的事件,证实了n-3多不饱和脂肪酸在感染不同阶段对免疫抵抗的损害。然而,我们推测其他细胞因子的调节也一定参与了这种反应,因为在单核细胞增生乳杆菌感染的晚期,饲喂鱼油的小鼠的细胞因子产生的变化与饲喂鱼油的小鼠相似,而后者从脾脏中清除这种细菌的能力得到了提高。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Assessment of interleukin-12, gamma interferon, and tumor necrosis factor alpha secretion in sera from mice fed with dietary lipids during different stages of Listeria monocytogenes infection.

Recent experimental observations have determined that long-chain n-3 polyunsaturated fatty acids suppress immune functions and are involved in the reduction of infectious disease resistance. BALB/c mice were fed for 4 weeks with one of four diets containing either olive oil (OO), fish oil (FO), hydrogenated coconut oil, or a low fat level. Interleukin-12p70 (IL-12p70), gamma interferon (IFN-gamma), and tumor necrosis factor alpha (TNF-alpha) production in the sera of mice fed these diets and challenged with Listeria monocytogenes were determined by enzyme-linked immunosorbent assay. In addition, bacterial counts from spleens of mice were carried out at 24, 72, or 96 h of infection. Here, we quantified an initial diminution of production of both IL-12p70 and IFN-gamma, which appear to play an important role in the reduction of host resistance to L. monocytogenes infection. In addition, an efficient elimination of L. monocytogenes was observed in spleens of mice fed a diet containing OO at 96 h of infection, despite reductions in IL-12p70 and TNF-alpha production, suggesting an improvement of immune resistance. Overall, our results indicate that the initial reduction of both IL-12 and IFN-gamma production before L. monocytogenes infection represents the most relevant event that corroborates the impairment of immune resistance by n-3 polyunsaturated fatty acids during the different stages of infection. However, we speculate that the modulation of other cytokines must be also involved in this response, because the alteration of cytokine production in mice fed an FO diet in a late phase of L. monocytogenes infection was similar to that in mice fed OO, whereas the ability to eliminate this bacterium from the spleen was improved in the latter group.

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