Functional alterations of myeloid cell subsets in hyperlipidaemia: relevance for atherosclerosis

Abstract

Atherosclerosis is a chronic inflammatory disease wherein the infiltration of myeloid cells of the vessel wall is a hallmark event. Lymphocytes, platelets and endothelial cells stand out as prominent suspects being involved in atherosclerosis. However, recent advances suggest a crucial role for myeloid leucocytes, specifically monocyte subsets, neutrophils, dendritic cells and endothelial progenitor cells. These cell types are not just rapidly recruited or already reside in the vascular wall, but also initiate and perpetuate core mechanisms in plaque formation and destabilization. Hyperlipidaemia is an independent risk factor for atherosclerosis. Herein, hyperlipidaemia skews myeloid cell haemostasis, phenotype and transcriptional regulation of pro-inflammatory factors ultimately promoting myeloid cell extravasation and atherosclerosis. We here review the role of myeloid cells in atherosclerosis as well as the effects of hyperlipidaemia on these cells.

Transcript origin analysis identifies antigen-presenting cells as primary targets of socially regulated gene expression in leukocytes

“…APCs produce the immediate inflammatory response to tissue damage that initiates immune responses (15,23). However, long-term or recurrent inflammation also promotes the chronic diseases that dominate "modern mortality," including atherosclerosis in cardiovascular disease (24,25), cancer initiation and metastasis (26,27), and neurodegeneration (10). The APC transcriptional activation observed here is consistent with previous data showing increased inflammatory gene expression in lonely individuals (4) and in people confronting a diverse array of other social adversities (1-3), suggesting a molecular basis for epidemiological links between social adversity and inflammation-mediated heart disease (11,28).…”

Multiple Roles for Neutrophils in Atherosclerosis

“…1,2 These two are interconnected as hypercholesterolemia increases circulating monocyte counts and renders these cells more prone for emigration into atherosclerotic lesions. 3 Hence, the causal contribution of monocytes and their descendants to atherosclerotic plaque formation, progression, and destabilization has been studied extensively. In addition, the contribution of immune cells such as T lymphocytes, mast cells, dendritic cells, and platelets to atherosclerosis has been firmly established over the years.…”

MCV and MCH Values in Coronary Artery Patients with Positive Gensini Score

“…Results of animal model research also showed that neutrophils contribute to the formation of atherosclerotic lesions (11,12). In addition, neutrophils were suggested to be critical in the progression phase of atherosclerosis (13). In another study, an increase was observed in oxidative activity and neutrophil aggression in coronary sinus of patients with CAD (14).…”