期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
卷 1841, 期 9, 页码 1329-1335出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbalip.2014.06.007
关键词
Beta-oxidation; Interleukin; Macrophages; Mitochondrial metabolism; Transcription coactivators
资金
- Deutsche Forschungsgemeinschaft [BR999, SFB 1039]
- Else Kroner Fresenius Foundation (Translational Research Innovation-Pharma, TRIP)
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-gamma co-activator 1 alpha/beta (PGC-1 alpha/beta), 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. (C) 2014 Elsevier B.V. All rights reserved.
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