首页> 美国卫生研究院文献>British Journal of Experimental Pathology >Cytokine release from human peripheral blood leucocytes incubated with endotoxin with and without prior infection with influenza virus: relevance to the sudden infant death syndrome.
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Cytokine release from human peripheral blood leucocytes incubated with endotoxin with and without prior infection with influenza virus: relevance to the sudden infant death syndrome.

机译:人内外周血白细胞释放的细胞因子释放后与有或没有事先感染流感病毒的内毒素一起培养:与婴儿猝死综合征有关。

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摘要

Previous work with a neonatal ferret model for human SIDS had indicated that inflammation caused by a combination of influenza virus and bacterial endotoxin may be a cause of human SIDS. To determine whether cytokines may be involved in this inflammatory response, levels of interleukin (IL)-1 beta, IL-6 and tumour necrosis factor (TNF)-alpha were examined, using ELISA assays, in culture supernatants of human peripheral blood leucocytes infected with influenza virus and subsequently incubated with endotoxin. Levels of TNF-alpha were increased compared to cells incubated with virus or endotoxin alone. Levels of IL-1 beta were also increased whereas levels of IL-6 were generally not enhanced. Cytokines appeared within 1-2 h of stimulation with virus or endotoxin and increased subsequently to reach maximum titres between 16 and 20 h post treatment. While levels of cytokine were much lower when determined using bioassays rather than ELISA assays, the pattern of increased yields from cells incubated with virus and endotoxin compared with either alone was still evident. The possible importance of these observations for SIDS victims is discussed.
机译:先前针对人类SIDS的新生儿雪貂模型所做的工作表明,由流感病毒和细菌内毒素共同引起的炎症可能是人类SIDS的原因。为了确定这种炎性反应是否可能涉及细胞因子,使用ELISA法在感染的人外周血白细胞的培养上清液中检查了白介素(IL)-1β,IL-6和肿瘤坏死因子(TNF)-α的水平用流感病毒,然后与内毒素一起孵育。与仅与病毒或内毒素孵育的细胞相比,TNF-α的水平增加。 IL-1β的水平也增加了,而IL-6的水平通常没有增加。细胞因子在被病毒或内毒素刺激后1-2小时内出现,并随后增加,在治疗后16至20小时达到最大滴度。虽然使用生物测定法而非ELISA测定法测定的细胞因子水平要低得多,但与单独使用病毒和内毒素孵育的细胞相比,细胞增产的模式仍然很明显。讨论了这些观察对小岛屿发展中国家受害者的可能重要性。

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