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首页> 外文期刊>Cell metabolism >Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages
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Metabolic dysfunction drives a mechanistically distinct proinflammatory phenotype in adipose tissue macrophages

机译：代谢功能障碍驱动脂肪组织巨噬细胞发生机械性不同的促炎表型

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Adipose tissue macrophage (ATM)-driven inflammation plays a key role in insulin resistance; however, factors activating ATMs are poorly understood. Using a proteomics approach, we show that markers of classical activation are absent on ATMs from obese humans but are readily detectable on airway macrophages of patients with cystic fibrosis, a disease associated with chronic bacterial infection. Moreover, treating macrophages with glucose, insulin, and palmitate - conditions characteristic of the metabolic syndrome - produces a "metabolically activated" phenotype distinct from classical activation. Markers of metabolic activation are expressed by proinflammatory ATMs in obese humans/mice and are positively correlated with adiposity. Metabolic activation is driven by independent proinflammatory and anti-inflammatory pathways, which regulate balance between cytokine production and lipid metabolism. We identify PPARγ and p62/SQSTM1 as two key proteins that promote lipid metabolism and limit inflammation in metabolically activated macrophages. Collectively, our data provide important mechanistic insights into pathways that drive the metabolic-disease-specific phenotype of macrophages.
机译：脂肪组织巨噬细胞（ATM）驱动的炎症在胰岛素抵抗中起关键作用。但是，激活ATM的因素了解得很少。使用蛋白质组学方法，我们显示肥胖人的ATM上不存在经典激活的标记，但在患有慢性细菌感染的囊性纤维化患者的气道巨噬细胞上很容易检测到。此外，用葡萄糖，胰岛素和棕榈酸酯治疗巨噬细胞-代谢综合征的特征-产生不同于经典激活的“代谢激活”表型。代谢激活的标志物在肥胖的人/小鼠中由促炎性ATM表达，并与肥胖呈正相关。代谢激活是由独立的促炎和抗炎途径驱动的，它们调节细胞因子产生和脂质代谢之间的平衡。我们确定PPARγ和p62 / SQSTM1是两个关键蛋白，它们促进脂质代谢并限制代谢激活的巨噬细胞中的炎症。总的来说，我们的数据为驱动巨噬细胞代谢疾病特异性表型的途径提供了重要的机制见解。

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