3 years ago

Postprandial triglyceride-rich lipoproteins promote lipid accumulation and apolipoprotein B-48 receptor transcriptional activity in human circulating and murine bone marrow neutrophils in a fatty acid-dependent manner

Postprandial triglyceride-rich lipoproteins promote lipid accumulation and apolipoprotein B-48 receptor transcriptional activity in human circulating and murine bone marrow neutrophils in a fatty acid-dependent manner
Rocío Abia, Beatriz Bermúdez, Sergio López, Francisco J.G. Muriana, Rosario Sánchez, Almudena Ortega-Gómez, Lourdes M. Varela, Sergio Montserrat de la Paz
Scope Postprandial triglyceride-rich lipoproteins (TRLs) promote atherosclerosis. Recent research points the bone marrow (BM) as a primary site in atherosclerosis. We elucidated how the acute administration of monounsaturated fatty acids (MUFAs) MUFAs, omega-3 polyunsaturated fatty acids (PUFAs) PUFAs and saturated fatty acids (SFAs) affects human circulating and murine BM neutrophil lipid accumulation and functionality. Methods and results Postprandial hypertriglyceridemia was induced in healthy subjects and Apoe−/− mice by the acute administration of dietary fats enriched in MUFAs, PUFAs, or SFAs. Postprandial hypertriglyceridemia increased apolipoprotein-B48 receptor (ApoB48R) transcriptional activity that was linearly correlated with intracellular triglycerides (TGs) TGs accumulation in human circulating and murine BM neutrophils. MUFA and omega-3 PUFAs attenuated ApoB48R gene expression and intracellular TG accumulation compared to SFAs. TRLs induced apoB48R-dependent TG accumulation in human neutrophils ex vivo. Murine BM neutrophils showed a decrease in surface L-selectin and an increase in TNF-α and IL-1β mRNA expressions only after SFAs administration. TRLs enriched in SFAs induced BM neutrophil degranulation ex vivo suggesting cell priming/activation. Conclusion Postprandial TRLs disrupts the normal biology and function of circulating and BM neutrophils. MUFA- and omega-3 PUFA-rich dietary fats such as virgin olive oil or fish oil has the potential to prevent excessive neutrophil lipid accumulation and activation by targeting the fatty acid composition of TRLs. Postprandial hypertriglyceridemia may contribute to atherosclerosis by promoting triglyceride rich lipoproteins (TRLs)-induced triglyceride accumulation and lipid droplets (LDs) formation via apoB48R in circulating and bone marrow (BM) neutrophils. In the BM, the acute ingestion of dietary fats rich in saturated fatty acids (SFAs) induce activation of BM neutrophils by decreasing CD62L surface expression and by increasing mRNA levels of IL-1β and TNF-α and by causing TRL-induced MMP9 release. MUFA oleic acid and omega-3 PUFAs counteract these effects.

Publisher URL: http://onlinelibrary.wiley.com/resolve/doi

DOI: 10.1002/mnfr.201600879

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