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Biology (Basel). 2015 Apr 9;4(2):314-26. doi: 10.3390/biology4020314.

Effect of Different Omega-6/Omega-3 Polyunsaturated Fatty Acid Ratios on the Formation of Monohydroxylated Fatty Acids in THP-1 Derived Macrophages.

Author information

1
Department of Medicine, Division of Hepatology, Gastroenterology and Endocrinology, Charité University Medicine Berlin, Campus Virchow-Klinikum, Berlin 13353, Germany. KeerenK@rki.de.
2
Department of Medicine, Division of Hepatology, Gastroenterology and Endocrinology, Charité University Medicine Berlin, Campus Virchow-Klinikum, Berlin 13353, Germany. dan.huang@charite.de.
3
Department of Medicine, Division of Hepatology, Gastroenterology and Endocrinology, Charité University Medicine Berlin, Campus Virchow-Klinikum, Berlin 13353, Germany. christopher.smyl@charite.de.
4
Lipid Clinic, Experimental and Clinical Research Centre (ECRC), Charité University Medicine and Max Delbrueck Center for Molecular Medicine, Berlin 13353, Germany. christopher.smyl@charite.de.
5
Department of Medicine, Division of Hepatology, Gastroenterology and Endocrinology, Charité University Medicine Berlin, Campus Virchow-Klinikum, Berlin 13353, Germany. andi.fischer@charite.de.
6
Lipidomix GmbH, Berlin 13125, Germany. michael.rothe@lipidomix.de.
7
Department of Medicine, Division of Hepatology, Gastroenterology and Endocrinology, Charité University Medicine Berlin, Campus Virchow-Klinikum, Berlin 13353, Germany. karsten.weylandt@charite.de.
8
Lipid Clinic, Experimental and Clinical Research Centre (ECRC), Charité University Medicine and Max Delbrueck Center for Molecular Medicine, Berlin 13353, Germany. karsten.weylandt@charite.de.

Abstract

Omega-6 and omega-3 polyunsaturated fatty acids (n-6 and n-3 PUFA) can modulate inflammatory processes. In western diets, the content of n-6 PUFA is much higher than that of n-3 PUFA, which has been suggested to promote a pro-inflammatory phenotype. The aim of this study was to analyze the effect of modulating the n-6/n-3 PUFA ratio on the formation of monohydroxylated fatty acid (HO-FAs) derived from the n-6 PUFA arachidonic acid (AA) and the n-3 PUFAs eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in THP-1 macrophages by means of LC-MS. Lipid metabolites were measured in THP-1 macrophage cell pellets. The concentration of AA-derived hydroxyeicosatetraenoic acids (HETEs) was not significantly changed when incubated THP-1 macrophages in a high AA/(EPA+DHA) ratio of 19/1 vs. a low ratio AA/(EPA+DHA) of 1/1 (950.6 ± 110 ng/mg vs. 648.2 ± 92.4 ng/mg, p = 0.103). Correspondingly, the concentration of EPA-derived hydroxyeicosapentaenoic acids (HEPEs) and DHA-derived hydroxydocosahexaenoic acids (HDHAs) were significantly increased (63.9 ± 7.8 ng/mg vs. 434.4 ± 84.3 ng/mg, p = 0.012 and 84.9 ± 18.3 ng/mg vs. 439.4 ± 82.7 ng/mg, p = 0.014, respectively). Most notable was the strong increase of 18-hydroxyeicosapentaenoic acid (18-HEPE) formation in THP-1 macrophages, with levels of 170.9 ± 40.2 ng/mg protein in the high n-3 PUFA treated cells. Thus our data indicate that THP-1 macrophages prominently utilize EPA and DHA for monohydroxylated metabolite formation, in particular 18-HEPE, which has been shown to be released by macrophages to prevent pressure overload-induced maladaptive cardiac remodeling.

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