Dietary Intake Regulates the Circulating Inflammatory Monocyte Pool

Stefan Jordan, Navpreet Tung, M. Casanova-Acebes, Christie Chang, Claudia Cantoni, Dachuan Zhang, Theresa H. Wirtz, Shruti Naik, Samuel A. Rose, Chad N. Brocker, Anastasiia Gainullina, Daniel Hornburg, Sam Horng, Barbara B. Maier, P. Cravedi, D. LeRoith, Frank J. Gonzalez, F. Meissner, J. Ochando, A. RahmanJerry E. Chipuk, Maxim N. Artyomov, Paul S. Frenette, L. Piccio, Marie Luise Berres, Emily J. Gallagher, Miriam Merad

Research output: Contribution to journalArticlepeer-review

245 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)1102-1114.e17
Issue number5
StatePublished - Aug 22 2019


  • AMPK
  • CCL2
  • Caloric restriction
  • PPARα
  • fasting
  • inflammation
  • inflammatory disease
  • liver
  • metabolism
  • monocyte

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology


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