首页> 外文期刊>American Journal of Physiology >Substance P enhances NF-kB transactivation and chemokine response in murine macrophages via ERK1/2 and p38 MAPK signaling pathways
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Substance P enhances NF-kB transactivation and chemokine response in murine macrophages via ERK1/2 and p38 MAPK signaling pathways

机译:P物质通过ERK1 / 2和p38 MAPK信号通路增强鼠巨噬细胞中的NF-kB反式激活和趋化因子反应

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摘要

neuro-immune interaction has been suggested to play a mod-ulatory role in a variety of immune and inflammatory conditions. The neuropeptide substance P (SP) has received considerable attention as a major mediator of neurogenic regulation of inflammation. SP belongs to the excitatory nonadrenergic, noncholinergic tachykinin family of peptides that elicit biological responses in effector cells through at least three distinct G protein-coupled receptors, the neurokinin (NK)-1, NK-2, and NK-3 receptors (44). SP exerts profound influence on inflammatory responses by affecting multiple aspects of immune cell function (38,44). In macrophages, SP is known to augment the production of cytokines such as interleukin (IL)-6 and tumor necrosis factor (TNF)-a via its COOH terminus (30).
机译:已经表明,神经-免疫相互作用在多种免疫和炎性疾病中起调节作用。神经肽物质P(SP)作为炎症的神经原性调节的主要介体已受到相当多的关注。 SP属于兴奋性非肾上腺素能,非胆碱能性速激肽家族的肽,通过至少三个不同的G蛋白偶联受体,神经激肽(NK)-1,NK-2和NK-3受体在效应细胞中引起生物反应(44) 。 SP通过影响免疫细胞功能的多个方面,对炎症反应产生深远的影响(38,44)。在巨噬细胞中,已知SP通过其COOH末端增加细胞因子(如白介素(IL)-6和肿瘤坏死因子(TNF)-a)的产生(30)。

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