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Triacylglycerol synthesis enhances macrophage inflammatory function

Author

Listed:
  • Angela Castoldi

    (Max Planck Institute of Epigenetics and Immunobiology)

  • Lauar B. Monteiro

    (Max Planck Institute of Epigenetics and Immunobiology
    University of Campinas)

  • Nikki van Teijlingen Bakker

    (Max Planck Institute of Epigenetics and Immunobiology
    University of Freiburg)

  • 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
    University of Freiburg)

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.

Suggested Citation

  • 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 G, 2020. "Triacylglycerol synthesis enhances macrophage inflammatory function," Nature Communications, Nature, vol. 11(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-17881-3
    DOI: 10.1038/s41467-020-17881-3
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