美国麻省总医院和哈佛医学院Filip K. Swirski研究组发现，单核细胞在禁食期间重新进入骨髓，改变宿主对感染的应答。相关论文于2023年2月23日发表在《免疫》杂志上。

他们发现了禁食诱导的白细胞迁移开关，该开关延长了单核细胞的寿命并改变了小鼠对疾病的易感性。他们表明，在活跃期禁食诱导单核细胞从血液快速返回骨髓。单核细胞再入由下丘脑-垂体-肾上腺（HPA）轴依赖性皮质酮释放协调，从而增强CXCR4趋化因子受体。虽然在营养匮乏期间，骨髓是单核细胞的避风港，但重新喂养促使动员，最终导致按时间顺序更老且转录不同的单核细胞的单核细胞增多。这些变化改变了对感染的应答。他们的研究表明，饮食 - 特别是饮食的时间动态平衡 - 调节单核细胞的寿命，从而适应外部压力源。

据悉，饮食明显地影响生理学。虽然营养过剩通过影响免疫力和新陈代谢来增加疾病风险，但热量限制和禁食似乎是有益的。尽管在饮食和健康之间观察到多种相关性，但潜在的生物学仍然不清楚。

附：英文原文

Title: Monocytes re-enter the bone marrow during fasting and alter the host response to infection

Author: Henrike Janssen, Florian Kahles, Dan Liu, Jeffrey Downey, Laura L. Koekkoek, Vladimir Roudko, Darwin D’Souza, Cameron S. McAlpine, Lennard Halle, Wolfram C. Poller, Christopher T. Chan, Shun He, John E. Mindur, Máté G. Kiss, Sumnima Singh, Atsushi Anzai, Yoshiko Iwamoto, Rainer H. Kohler, Kashish Chetal, Ruslan I. Sadreyev, Ralph Weissleder, Seunghee Kim-Schulze, Miriam Merad, Matthias Nahrendorf, Filip K. Swirski

Issue&Volume: 2023-02-23

Abstract: Diet profoundly influences physiology. Whereas over-nutrition elevates risk for diseasevia its influence on immunity and metabolism, caloric restriction and fasting appearto be salutogenic. Despite multiple correlations observed between diet and health,the underlying biology remains unclear. Here, we identified a fasting-induced switchin leukocyte migration that prolongs monocyte lifespan and alters susceptibility todisease in mice. We show that fasting during the active phase induced the rapid returnof monocytes from the blood to the bone marrow. Monocyte re-entry was orchestratedby hypothalamic-pituitary-adrenal (HPA) axis-dependent release of corticosterone,which augmented the CXCR4 chemokine receptor. Although the marrow is a safe havenfor monocytes during nutrient scarcity, re-feeding prompted mobilization culminatingin monocytosis of chronologically older and transcriptionally distinct monocytes.These shifts altered response to infection. Our study shows that diet—in particular,a diet’s temporal dynamic balance—modulates monocyte lifespan with consequences foradaptation to external stressors.

DOI: 10.1016/j.immuni.2023.01.024

Source: https://www.cell.com/immunity/fulltext/S1074-7613(23)00036-5