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首页> 外文期刊>Cell metabolism >Linking Lipid Metabolism to the Innate Immune Response in Macrophages through Sterol Regulatory Element Binding Protein-1a.
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Linking Lipid Metabolism to the Innate Immune Response in Macrophages through Sterol Regulatory Element Binding Protein-1a.

机译：通过甾醇调节因子结合蛋白-1a将脂质代谢与巨噬细胞的先天免疫反应联系起来。

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摘要

We show that mice with a targeted deficiency in the gene encoding the lipogenic transcription factor SREBP-1a are resistant to endotoxic shock and systemic inflammatory response syndrome induced by cecal ligation and puncture (CLP). When macrophages from the mutant mice were challenged with bacterial lipopolysaccharide, they failed to activate lipogenesis as well as two hallmark inflammasome functions, activation of caspase-1 and secretion of IL-1beta. We show that SREBP-1a activates not only genes required for lipogenesis in macrophages but also the gene encoding Nlrp1a, which is a core inflammasome component. Thus, SREBP-1a links lipid metabolism to the innate immune response, which supports our hypothesis that SREBPs evolved to regulate cellular reactions to external challenges that range from nutrient limitation and hypoxia to toxins and pathogens.
机译：我们显示具有编码脂肪生成转录因子SREBP-1a的基因中有针对性的小鼠对盲肠结扎和穿刺（CLP）诱导的内毒素休克和全身炎症反应综合征具有抵抗力。当来自突变小鼠的巨噬细胞受到细菌脂多糖的攻击时，它们无法激活脂肪生成以及两种标志性的炎性体功能：caspase-1的激活和IL-1beta的分泌。我们显示，SREBP-1a不仅激活巨噬细胞中脂肪生成所需的基因，而且还激活编码Nlrp1a的基因，Nlrp1a是核心炎症小体成分。因此，SREBP-1a将脂质代谢与先天免疫反应联系起来，这支持了我们的假设，即SREBPs进化为调节细胞反应以应对从营养限度和低氧到毒素和病原体的外部挑战。

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