Macrophage Foam Cells

Abstract

Abstract Foam cells are lipid‐loaded macrophages that are generated from the massive uptake of modified low‐density lipoproteins and the intracytoplasmatic accumulation of cholesteryl esters. Foam cells are present in all stages of atherosclerosis and participate in inflammatory responses and tissue remodelling within the arterial intima. Foam cells can also be generated as a consequence of infection by persistent pathogens, such as Mycobacterium , Chlamydia and Toxoplasma . These pathogens meet nutritional advantages by residing within cells that accumulate lipids. When the immune system is unable to eliminate substances perceived as foreign, it produces a granuloma, composed mostly of macrophages, attempting to wall off the non‐self material. This article reviews the processes that lead to the regulation of foam cell formation in atherosclerosis and infection. Key Concepts Foam cells are lipid‐loaded macrophages. Foam cells are generated upon massive uptake of modified low‐density lipoproteins and the intracellular accumulation of cholesteryl esters. Foam cells form during development of atherosclerosis and as a result of different infections. Foam cells participate in inflammatory responses and tissue remodelling. Endothelial transmigration of monocytes is the first step in the development of atherosclerosis. Once monocytes reach the arterial wall intima, they undergo phenotypic transformation into macrophages, internalise large amounts of modified LDLs and become foam cells. Heterodimers of liver X receptors (LXR) and retinoid X receptors (RXR) directly upregulate the expression of several genes involved in lipid and lipoprotein homeostasis. When the immune system is unable to eliminate substances perceived as foreign, it produces a granuloma, composed mostly of macrophages, that attempts to wall off the non‐self material.