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Biochim Biophys Acta. 2014 Sep;1841(9):1329-35. doi: 10.1016/j.bbalip.2014.06.007. Epub 2014 Jun 21.

Fatty acid oxidation is dispensable for human macrophage IL-4-induced polarization.

Author information

1
Goethe-University Frankfurt, Faculty of Medicine, Institute of Biochemistry I/ZAFES, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany.
2
Goethe-University Frankfurt, Faculty of Medicine, Institute of Biochemistry I/ZAFES, Theodor-Stern-Kai 7, 60590 Frankfurt, Germany. Electronic address: bruene@pathobiochemie1.de.

Abstract

Macrophage polarization elicits various metabolic alterations which in turn influence the polarized phenotype. Activation of glycolytic metabolism accompanies and supports macrophage pro-inflammatory M1 polarization. In contrast, M2 polarization of murine macrophages in response to the Th2 cytokine interleukin-4 (IL-4) was linked to the up-regulation of mitochondrial oxidative metabolism and fatty acid oxidation (FAO), which was necessary for coining an IL-4-polarized phenotype. Here we investigated whether similar mechanisms operate in human macrophages stimulated with IL-4. IL-4 causes only moderate changes of mitochondrial oxidative metabolism and FAO, correlating with an unaltered expression of peroxisome proliferator-activated receptor-γ coactivator 1 α/β (PGC-1α/β), the master transcriptional regulators of mitochondrial biogenesis. Furthermore, attenuating FAO had no effect on IL-4-induced polarization-associated gene expression. Apparently, FAO is dispensable for IL-4-induced polarization of human macrophages, pointing to fundamental differences in the metabolic requirements of macrophage phenotype alterations between mice and humans.

KEYWORDS:

Beta‐oxidation; Interleukin; Macrophages; Mitochondrial metabolism; Transcription coactivators

PMID:
24960101
DOI:
10.1016/j.bbalip.2014.06.007
[Indexed for MEDLINE]

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