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非传统细胞因子:儿茶酚胺和脂肪因子如何在免疫、代谢及中枢神经系统中影响巨噬细胞

Non-traditional cytokines: How catecholamines and adipokines influence macrophages in immunity, metabolism and the central nervous system.

作者信息

Barnes Mark A, Carson Monica J, Nair Meera G

机构信息

Division of Biomedical Sciences, School of Medicine, University of California Riverside, Riverside, CA, United States.

Division of Biomedical Sciences, School of Medicine, University of California Riverside, Riverside, CA, United States.

出版信息

Cytokine. 2015 Apr;72(2):210-9. doi: 10.1016/j.cyto.2015.01.008. Epub 2015 Feb 18.

Abstract

Catecholamines and adipokines function as hormones; catecholamines as neurotransmitters in the sympathetic nervous system, and adipokines as mediators of metabolic processes. It has become increasingly clear, however, that both also function as immunomodulators of innate and adaptive immune cells, including macrophages. Macrophages can respond to, as well as produce their own catecholamines. Dopamine, noradrenaline, and adrenaline are the most abundant catecholamines in the body, and can induce both pro-inflammatory and anti-inflammatory immune responses in macrophages, as well as non-immune processes such as thermogenesis. Though they are responsive to adipokines, particularly lipoproteins, leptin, and adiponectin, macrophages generally do not synthesize their own adipokines, with the exception being resistin-like molecules. Adipokines contribute to adverse metabolic and immune responses by stimulating lipid accumulation, foam cell formation and pro-inflammatory cytokine production in macrophages. Adipokines can also promote balance or resolution during metabolic and immune processes by promoting reverse lipid transport and expression of Th2 cytokines. This review will explore the mechanisms by which catecholamines and adipokines influence macrophage function in neural pathways, immunity and metabolism.

摘要

儿茶酚胺和脂肪因子具有激素功能;儿茶酚胺在交感神经系统中作为神经递质,脂肪因子作为代谢过程的介质。然而,越来越清楚的是,它们两者也作为先天性和适应性免疫细胞(包括巨噬细胞)的免疫调节剂发挥作用。巨噬细胞既能对儿茶酚胺作出反应,也能产生自身的儿茶酚胺。多巴胺、去甲肾上腺素和肾上腺素是体内最丰富的儿茶酚胺,它们既能在巨噬细胞中诱导促炎和抗炎免疫反应,也能诱导诸如产热等非免疫过程。巨噬细胞虽然对脂肪因子,特别是脂蛋白、瘦素和脂联素产生反应,但一般不合成自身的脂肪因子,抵抗素样分子除外。脂肪因子通过刺激巨噬细胞中的脂质积累、泡沫细胞形成和促炎细胞因子产生,导致不良的代谢和免疫反应。脂肪因子还可以通过促进逆向脂质转运和Th2细胞因子的表达,在代谢和免疫过程中促进平衡或恢复。本综述将探讨儿茶酚胺和脂肪因子在神经通路、免疫和代谢中影响巨噬细胞功能的机制。

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