Abstract
Toll-like receptors are well-defined barriers in innate immunity. Among them hTLR4 on the surface of monocytes, plays a critical role in the formation of atherosclerotic plaques, plaque instability and arterial remodeling through production of inflammatory cytokines. This study was designed to examine the association of hTLR4 monocyte expression and response with the severity of coronary stenosis in patients with stable angina (SA). Blood samples were obtained from 39 patients with SA who were scheduled for a coronary angiography and from 28 healthy volunteers. The samples were collected before the procedure. Expression of hTLR4 on CD14+ monocytes and serum levels of TNF-α and IL-1β were measured using flowcytometry and ELISA techniques respectively. Percentage stenosis diameter was measured by comparing the area of coronary stenosis to an adjacent normal segment of the vessel. Compared with control group, patients showed upregulation of hTLR4+/CD14+ monocytes. Furthermore, patients with more severe coronary stenosis exhibited enhanced expression of hTLR4+/CD14+ monocytes (p α (p β. In addition, significant correlations were seen between percentage stenosis diameter and monocyte expression of hTLR4 as well as TNF-α. hTLR4 monocytic expression and related cytokines are positively associated percentage stenosis diameter. These results suggest that hTLR4 activity may be involved in progression of atherosclerosis.
Highlights
Atherosclerosis is the main cause of cardiovascular mortality
In the present study we evaluated the expression of hTLR4 on peripheral CD14+ monocytes in patients with stable angina who were on standard medications
In thisinvestigation we used flowcytometry and enzyme-linked immunosorbent assay (ELISA) to describe an association between monocyte expression levels of hTLR4 and its related signaling events with percentage diameter stenosis of the coronary arteries
Summary
A significant body of evidence suggests that inflammation plays a key role in the formation of atherosclerotic plaques [1,2,3]. Toll like receptors (TLRs) are cell membrane receptors that are activated by different pathogen-associated molecular patterns (PAMPs) [4]. Ten functional human TLRs (hTLR) have been identified so far [5]. HTLR4 is well recognized in cardiovascular disease in the formation of atherosclerotic plaques [6,7]. It is documented that exogenous ligands like lipopolysaccharide (LPS) of bacteria, fungi and viruses can activate this receptor and cause immune responses [8]. It has been suggested that TNF-α is linked with myocardial infarction and may potentially harm coronary arteries [15].
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