Triacylglycerol synthesis enhances macrophage inflammatory function

Angela Castoldi, Lauar B. Monteiro, Nikki van Teijlingen Bakker, David E. Sanin, Nisha Rana, Mauro Corrado, Alanna M. Cameron, Fabian Hässler, Mai Matsushita, George Caputa, Ramon I. Klein Geltink, Jörg Büscher, Joy Edwards-Hicks, Erika L. Pearce and Edward J. Pearce ()
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Angela Castoldi: Max Planck Institute of Epigenetics and Immunobiology
Lauar B. Monteiro: Max Planck Institute of Epigenetics and Immunobiology
Nikki van Teijlingen Bakker: Max Planck Institute of Epigenetics and Immunobiology
David E. Sanin: Max Planck Institute of Epigenetics and Immunobiology
Nisha Rana: Max Planck Institute of Epigenetics and Immunobiology
Mauro Corrado: Max Planck Institute of Epigenetics and Immunobiology
Alanna M. Cameron: Max Planck Institute of Epigenetics and Immunobiology
Fabian Hässler: Max Planck Institute of Epigenetics and Immunobiology
Mai Matsushita: Max Planck Institute of Epigenetics and Immunobiology
George Caputa: Max Planck Institute of Epigenetics and Immunobiology
Ramon I. Klein Geltink: Max Planck Institute of Epigenetics and Immunobiology
Jörg Büscher: Max Planck Institute of Epigenetics and Immunobiology
Joy Edwards-Hicks: Max Planck Institute of Epigenetics and Immunobiology
Erika L. Pearce: Max Planck Institute of Epigenetics and Immunobiology
Edward J. Pearce: Max Planck Institute of Epigenetics and Immunobiology

Nature Communications, 2020, vol. 11, issue 1, 1-11

Abstract: Abstract Foamy macrophages, which have prominent lipid droplets (LDs), are found in a variety of disease states. Toll-like receptor agonists drive triacylglycerol (TG)-rich LD development in macrophages. Here we explore the basis and significance of this process. Our findings indicate that LD development is the result of metabolic commitment to TG synthesis on a background of decreased fatty acid oxidation. TG synthesis is essential for optimal inflammatory macrophage activation as its inhibition, which prevents LD development, has marked effects on the production of inflammatory mediators, including IL-1β, IL-6 and PGE2, and on phagocytic capacity. The failure of inflammatory macrophages to make PGE2 when TG-synthesis is inhibited is critical for this phenotype, as addition of exogenous PGE2 is able to reverse the anti-inflammatory effects of TG synthesis inhibition. These findings place LDs in a position of central importance in inflammatory macrophage activation.

Date: 2020
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-17881-3

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DOI: 10.1038/s41467-020-17881-3

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