美国西奈山伊坎医学院Miriam Merad、Stefan Jordan研究团队合作发现，饮食摄入量参与调控循环炎症单核细胞群体数量。2019年8月22日出版的《细胞》发表了这项成果。
研究人员发现，短期禁食减少单核细胞代谢和炎症活动，并大大减少循环单核细胞的数量。 外周单核细胞数量的调节取决于膳食葡萄糖和蛋白质水平。具体而言，研究人员发现肝细胞中低能量传感器AMPK（5′-AMP-activated protein kinase）的激活以及PPARα（peroxisome proliferator-activator receptor alpha）对全身CCL2产生的抑制减少了来自骨髓的单核细胞调动。重要的是，研究人员发现，禁食可改善慢性炎症性疾病，同时不会影响急性感染性炎症和组织修复过程中单核细胞的紧急调动。这些结果表明，热量摄入和肝脏能量传感器决定了血液和组织的免疫调节，并将饮食习惯与炎症性疾病的结果联系起来。
研究人员表示，限制热量可以改善炎症和自身免疫性疾病，但此前对热量摄入减少调节炎症的机制知之甚少。
附：英文原文
Title: Dietary Intake Regulates the Circulating Inflammatory Monocyte Pool
Author: Stefan Jordan,Navpreet Tung,Maria Casanova-Acebes,Christie Chang,Claudia Cantoni,Dachuan Zhang,Theresa H. Wirtz,Shruti Naik,Samuel A. Rose,Chad N. Brocker,Anastasy?yiia Gainullina,Daniel Hornburg,Sam Horng,Barbara B. Maier,Paolo Cravedi,Derek LeRoith,Frank J. Gonzalez,Felix Meissner,Jordi Ochando,Adeeb Rahman,Jerry E. Chipuk,Maxim N. Artyomov,Paul S. Frenette,Laura Piccio,Marie-Luise Berres,Emily J. Gallagher,Miriam Merad
Issue&Volume:Volume 178 Issue 5
Abstract: Caloric restriction is known to improve inflammatory and autoimmune diseases. However, the mechanisms by which reduced caloric intake modulates inflammation are poorly understood. Here we show that short-term fasting reduced monocyte metabolic and inflammatory activity and drastically reduced the number of circulating monocytes. Regulation of peripheral monocyte numbers was dependent on dietary glucose and protein levels. Specifically, we found that activation of the low-energy sensor 5′-AMP-activated protein kinase (AMPK) in hepatocytes and suppression of systemic CCL2 production by peroxisome proliferator-activator receptor alpha (PPARα) reduced monocyte mobilization from the bone marrow. Importantly, we show that fasting improves chronic inflammatory diseases without compromising monocyte emergency mobilization during acute infectious inflammation and tissue repair. These results reveal that caloric intake and liver energy sensors dictate the blood and tissue immune tone and link dietary habits to inflammatory disease outcome.
DOI: https://doi.org/10.1016/j.cell.2019.07.050
Source: https://www.cell.com/cell/fulltext/S0092-8674(19)30850-5