Heart Care Info - Heart Disease Prevention & Treatment

Nur77turing Macrophages in Atherosclerosis

P Lefebvre, G Chinetti... - Circulation Research, 2012 - Am Heart Assoc Inflammation often initiates by the recruitment of neutro- phils and monocytes to the damaged tissue, a process normally rapidly terminated via, among others, the secretion of anti-inflammatory cytokines. An imbalance of inflamma- tion initiation and arrest results in chronic ... [HTML]

Inflammation often initiates by the recruitment of neutrophils and monocytes to the damaged tissue, a process normally rapidly terminated via, among others, the secretion of anti-inflammatory cytokines. An imbalance of inflammation initiation and arrest results in chronic inflammatory diseases, such as atherosclerosis, in which both innate and adaptive immune responses participate in response to risk factors, such as elevated lipoproteins.1 In the mouse, 2 major types of monocytes, Ly6 Chi and Ly6 Clow, circulate in blood.2 Ly6 Chi monocytes display a proinflammatory phenotype, whereas Ly6 Clow monocytes are patrolling cells monitoring vascular integrity and exerting, without extravasation, anti-inflammatory and tissue repair activities. Of note, hypercholesterolemia induces a predominant Ly6 Chi monocytosis, which gives rise to atherosclerotic lesion macrophages.3 Monocyte-derived macrophages are among the first immune cells detected in the developing atherosclerotic plaque. Recently, the macrophage population in human atherosclerotic plaques was also found to be heterogeneous4 and classified as proinflammatory “classical” M1 or anti-inflammatory “alternative” M2 macrophages. M1 macrophages are typically found in lipid-rich areas with necrosis, characterizing the unstable plaque, whereas M2 macrophages are enriched in lipid-poor zones of high cellularity.5 An imbalance in favor of the M1 phenotype could thus maintain a deleterious inflammatory state, whereas shifting toward the M2 phenotype would convey anti-inflammatory responses.