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首页> 外文期刊>The Journal of Immunology: Official Journal of the American Association of Immunologists >Inflammatory cytokines IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha impart neuroprotection to an excitotoxin through distinct pathways.
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Inflammatory cytokines IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha impart neuroprotection to an excitotoxin through distinct pathways.

机译：炎性细胞因子IL-1 alpha，IL-1 beta，IL-6和TNF-α通过不同的途径赋予神经兴奋性神经毒素保护作用。

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摘要

The proinflammatory cytokines IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha are produced within the CNS, and, similar to the periphery, they have pleotrophic and overlapping functions. We have shown previously that TNF-alpha increases neuronal survival to a toxic influx of calcium mediated through neuronal N-methyl-d -aspartic acid (NMDA) glutamate-gated ion channels. This process, termed excitotoxicity, is a major contributor to neuronal death following ischemia or stroke. Neuroprotection by this cytokine requires both activation of the p55/TNF receptor type I and the release of TNF-alpha from neurons, and it is inhibited by the plant alkaloid nicotine. Here, we report that other inflammatory cytokines (IL-1 alpha, IL-1 beta, and IL-6) are also neuroprotective to excessive NMDA challenge in our system. Neuroprotection provided by IL-1 is distinct from TNF-alpha because it is inhibited by IL-1 receptor antagonist; it is not antagonized by nicotine, but it is inhibited by a neutralizing Ab to nerve growth factor (NGF). Similar to IL-1, IL-6-mediated neuroprotection is also antagonized by pretreatment with IL-1 receptor antagonist and it is not affected by nicotine. However, neutralizing anti-NGF only partially blocks IL-6-mediated protection. These studies support an important role for distinct but overlapping neuroprotective cytokine effects in the CNS.
机译：促炎细胞因子IL-1α，IL-1β，IL-6和TNF-α在中枢神经系统内产生，并且类似于外周，它们具有肥大和重叠的功能。以前我们已经表明，TNF-α通过神经元N-甲基-d-天冬氨酸（NMDA）谷氨酸门控离子通道介导的钙离子流入增加了神经元存活。这一过程称为兴奋性毒性，是导致缺血或中风后神经元死亡的主要原因。通过这种细胞因子的神经保护作用既需要激活I型p55 / TNF受体，又需要从神经元释放TNF-α，并且被植物生物碱烟碱抑制。在这里，我们报道了其他炎性细胞因子（IL-1 alpha，IL-1 beta和IL-6）对我们系统中过量的NMDA攻击也具有神经保护作用。 IL-1提供的神经保护作用不同于TNF-α，因为它受到IL-1受体拮抗剂的抑制。它不受尼古丁拮抗，但被中和抗体对神经生长因子（NGF）抑制。与IL-1相似，IL-6介导的神经保护作用也受到IL-1受体拮抗剂的预处理而被拮抗，并且不受尼古丁的影响。然而，中和抗NGF仅部分阻断IL-6介导的保护。这些研究支持中枢神经系统中独特但重叠的神经保护细胞因子作用的重要作用。

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