Effects of a High-Fat Meal on the Inflammatory Phenotype and Function of Monocytes

Abstract

Cardiovascular disease (CVD) remains the leading cause of mortality throughout the world. Atherosclerosis, the buildup of plaque within the arteries, is the main cause of CVD. An early and essential step in the pathogenesis of atherosclerosis is the formation of foam cells, derived from lipid-laden macrophages that become trapped within the tunica intima. Macrophages, through the scavenger receptor CD36, take up a modified form of cholesterol, oxidized low-density lipoprotein (oxLDL), at a rapid rate, which causes them to become lipid-laden and trapped. Chronic inflammation causes endothelial damage and dysfunction, increasing the permeability to circulating LDL, which becomes oxidized within the arteries. Due to the difficulty of studying the macrophages within atherosclerotic plaque, recent research has shifted to the study of their biological precursor: monocytes. A high-fat meal (HFM), an experimental model used to assess postprandial inflammation, was used to assess the role of this HFM-induced inflammation on the likelihood of monocytes to eventually become foam cells. We also included an additional oxLDL ex vivo treatment to gain further insight into the potential “priming” effect of a single HFM. While there was a significant increase in the inflammatory cytokine tumor necrosis factor alpha (TNF-a) in response to the HFM, there were no significant changes in monocyte oxLDL uptake or cell surface marker expression. Future studies may want to examine the inflammatory role that higher concentrations of oxLDL may have or examine other postprandial markers of inflammation in an older or at-risk population.