Background: Atherosclerosis potentially represents a chronic inflammatory disease in which both endothelial cells and monocytes are involved. Monocyte-endothelium adhesion, which is heavily dependent on the expression of adhesion molecules, such as vascular cell adhesion molecule 1 (VCAM-1), is one of the key stages of atherogenesis. Toll-like receptor 4 (TLR4) has been found in atheroma and adventitia of human atherosclerotic coronary arteries. In TLR4-knockout mice studies, TLR4 contributes to atherogenesis via the nuclear factor-kappa B signal pathway, a process within which adhesion molecules are involved. Bacterial infection, such as Chlamydia pneumonia and lipopolysaccharide (LPS), is well known to act as the ligand of TLR4, triggering the overexpression of adhesion molecules and other inflammatory mediators, which can ultimately lead to atherogenesis. Purpose: In this study, we explore the role of TLR4 in the monocyte-endothelium adhesion. Method: The monocyte-endothelium adhesion triggered by LPS on human coronary artery endothelial cells was tested by anti-TLR4 antibody and anti-VCAM-1 antibody. Results: The inhibition of TLR4 could suppress the overexpression of VCAM-1 in messenger RNA and protein levels. Both anti-TLR4 antibody and anti-VCAM-1 antibody interfere with monocyte-endothelium adhesion. Conclusion: We conclude that LPS upregulates VCAM-1 by interacting with TLR4 and then enhances monocyte-endothelium adhesion. These findings may imply that the inhibition of TLR4 could be a potential target for atherosclerosis therapy.
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