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首页> 外文期刊>The European Journal of Neuroscience >Uncoupling of interleukin-6 from its signalling pathway by dietary n-3-polyunsaturated fatty acid deprivation alters sickness behaviour in mice.
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Uncoupling of interleukin-6 from its signalling pathway by dietary n-3-polyunsaturated fatty acid deprivation alters sickness behaviour in mice.

机译：饮食中的n-3-多不饱和脂肪酸剥夺使白介素6与信号传导途径脱钩，从而改变了小鼠的疾病行为。

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Sickness behaviour is an adaptive behavioural response to the activation of the innate immune system. It is mediated by brain cytokine production and action, especially interleukin-6 (IL-6). Polyunsaturated fatty acids (PUFA) are essential fatty acids that are highly incorporated in brain cell membranes and display immunomodulating properties. We hypothesized that a decrease in n-3 (also known as omega3) PUFA brain level by dietary means impacts on lipopolysaccharide (LPS)-induced IL-6 production and sickness behaviour. Our results show that mice exposed throughout life to a diet containing n-3 PUFA (n-3-6 diet) display a decrease in social interaction that does not occur in mice submitted to a diet devoid of n-3 PUFA (n-6 diet). LPS induced high IL-6 plasma levels as well as expression of IL-6 mRNA in the hippocampus and cFos mRNA in the brainstem of mice fed either diet, indicating intact immune-to-brain communication. However, STAT3 and STAT1 activation, a hallmark of the IL-6 signalling pathway, was lower in the hippocampus of LPS-treated n-6 mice than n-3-6 mice. In addition, LPS did not reduce social interaction in IL-6-knockout (IL-6-KO) mice and failed to induce STAT3 activation in the brain of IL-6-KO mice. Altogether, these findings point to alteration in brain STAT3 as a key mechanism for the lack of effect of LPS on social interaction in mice fed with the n-6 PUFA diet. The relative deficiency of Western diets in n-3 PUFA could impact on behavioural aspects of the host response to infection.
机译：疾病行为是对先天免疫系统激活的适应性行为反应。它是由脑细胞因子的产生和作用介导的，尤其是白介素6（IL-6）。多不饱和脂肪酸（PUFA）是必需脂肪酸，高度掺入脑细胞膜并显示免疫调节特性。我们假设通过饮食手段使n-3（也称为omega3）PUFA脑水平下降会影响脂多糖（LPS）诱导的IL-6产生和疾病行为。我们的结果表明，一生中暴露于含n-3 PUFA（n-3 / n-6饮食）饮食的小鼠表现出社交互动的减少，这在接受n-3 PUFA（n -6节食）。 LPS可以诱导高IL-6血浆水平以及饲喂两种饮食的小鼠海马中IL-6 mRNA的表达以及脑干cFos mRNA的表达，表明免疫-大脑的通讯是完整的。但是，STAT3和STAT1激活（IL-6信号通路的标志）在LPS处理的n-6小鼠的海马中比n-3 / n-6小鼠低。此外，LPS不会减少IL-6-KO小鼠（IL-6-KO）的社交互动，也无法诱导IL-6-KO小鼠的大脑中的STAT3激活。总而言之，这些发现表明大脑STAT3的改变是LPS对n-6 PUFA饮食喂养的小鼠缺乏社交互动影响的关键机制。 n-3 PUFA中西方饮食的相对缺乏可能会影响宿主对感染反应的行为方面。

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