Journal
CELL
Volume 178, Issue 5, Pages 1102-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2019.07.050
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Funding
- NIH [R01 CA154947, U24 AI118644, U19 AI128949, K08CA190770]
- Tisch Cancer Institute
- German Research Council (DFG) [SFB-TRR57 P07, JO 1216/1-1]
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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 hepato-cytes and suppression of systemic CCL2 production by peroxisome proliferator-activator receptor alpha (PPAR alpha) 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.
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