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Dietary Intake Regulates the Circulating Inflammatory Monocyte Pool

Author:
Jordan, Stefan, Tung, Navpreet, Casanova-Acebes, Maria, Chang, Christie, Cantoni, Claudia, Zhang, Dachuan, Wirtz, Theresa H., Naik, Shruti, Rose, Samuel A., Brocker, Chad N., Gainullina, Anastasiia, Hornburg, Daniel, Horng, Sam, Maier, Barbara B., Cravedi, Paolo, LeRoith, Derek, Gonzalez, Frank J., Meissner, Felix, Ochando, Jordi, Rahman, Adeeb, Chipuk, Jerry E., Artyomov, Maxim N., Frenette, Paul S., Piccio, Laura, Berres, Marie-Luise, Gallagher, Emily J., Merad, Miriam
Source:
Cell 2019 v.178 no.5 pp. 1102-1114.e17
ISSN:
0092-8674
Subject:
autoimmune diseases, bone marrow, chemokine CCL2, energy intake, fasting, food intake, glucose, hepatocytes, inflammation, liver, low calorie diet, monocytes, peroxisome proliferator-activated receptor alpha, protein content, protein kinases, tissue repair
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.
Agid:
6593159