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首页> 外文期刊>Journal of Cellular Physiology >Regulation of Cigarette Smoke Induction of IL-8 in Macrophages by AMP-activated Protein Kinase Signaling
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Regulation of Cigarette Smoke Induction of IL-8 in Macrophages by AMP-activated Protein Kinase Signaling

机译：规定引发的香烟烟雾感应巨噬细胞活化蛋白激酶信号

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Inhaled cigarette smoke (CS) causes persistent lung inflammation in smokers. Interleukin 8 (IL-8) released from macrophages is a key chemokine during initiation and progression of CS-induced lung inflammation, yet its regulation is largely unknown. AMP-activated protein kinase (AMPK), a crucial energy homeostasis regulator, may modulate inflammation. Here we report that CS extract (CSE) increased the level of intracellular reactive oxygen species (ROS), activating AMPK, mitogen-activated protein kinases (MAPKs), and NF-B, as well as inducing IL-8, in human macrophages. N-acetyl-cysteine (ROS scavenger) or hexamethonium [nicotinic acetylcholine receptor (nAChR) antagonist] attenuated the CSE-induced increase in intracellular ROS, activation of AMPK and NF-B, as well as IL-8 induction, which suggests that nAChRs and ROS are important. Prevention of AMPK activation by compound C or AMPK siRNA reduced CSE-induced IL-8 production, confirming the role of AMPK. Compound C or AMPK siRNA also inhibited the activation of MAPKs and NF-B by CSE, which suggests that these molecules are downstream of AMPK. Additionally, exposure of human macrophages to nicotine activated AMPK and induced IL-8 and that these effects were lessened by hexamethonium or compound C, implying that nicotine in CS may be causative. Furthermore, chronic CS exposure in mice promoted AMPK phosphorylation and expression of MIP-2 (an IL-8 homolog) in infiltrated macrophages and in lung tissues, as well as induced lung inflammation, all of which were reduced by compound C treatment. Thus, we identified a novel nAChRs-dependent, ROS-sensitive, AMPK/MAPKs/NF-B signaling pathway, which seems to be important to CS-induced macrophage IL-8 production and possibly to lung inflammation. J. Cell. Physiol. 230: 1781-1793, 2015. (c) 2014 Wiley Periodicals, Inc.
机译：吸入香烟烟雾(CS)造成持久的在吸烟者的肺部炎症。(引发)从巨噬细胞释放是一个关键趋化因子的发生和发展过程CS-induced肺部炎症,但其监管在很大程度上是未知的。体内平衡调节器(AMPK),一个至关重要的能量,可以调节炎症。提取物(CSE)增加的程度细胞内活性氧(ROS),激活AMPK,增殖作用激酶(MAPKs), NF-B以及诱导引发,在人类巨噬细胞。(活性氧清除剂)或六甲铵(烟碱乙酰胆碱受体(乙酰)拮抗剂)减毒CSE-induced增加细胞内ROS,激活AMPK和NF-B以及引发感应,这表明乙酰和ROS是很重要的。由复合C或激活AMPK siRNA减少CSE-induced引发生产,确认所扮演的角色AMPK。激活MAPKs和NF-B CSE,表明,这些分子的下游AMPK。对尼古丁激活AMPK和诱导引发这些影响被六甲铵减少或复合C,这意味着在CS尼古丁可能使役动词。老鼠提升AMPK磷酸化和表达MIP-2(一个引发同族体)的渗透巨噬细胞在肺组织,以及引起肺部炎症,所有这一切减少复合C治疗。确定了小说nAChRs-dependent,ROS-sensitive, AMPK / MAPKs / NF-B信号通路,这似乎是重要CS-induced吗肺巨噬细胞引发生产和可能炎症。2015.

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