Eikenella corrodens is a gram‐negative bacterium, and although primarily associated with periodontal infections or infective endocarditis, it has been identified in coronary atheromatous plaques. The effect of its lipopolysaccharide ( LPS ) on human coronary artery endothelial cells ( HCAEC s) is unknown. Our aim was to examine the mechanism underlying the inflammatory response in HCAEC s stimulated with E. corrodens‐ LPS and to evaluate monocyte adhesion. Endothelial responses were determined by measuring the levels of chemokines and cytokines using flow cytometry. The surface expression of intercellular adhesion molecule 1 ( ICAM ‐1) was determined using a cell‐based ELISA , and the adhesion of THP ‐1 monocytes to HCAEC s was also monitored. The involvement of toll‐like receptors ( TLRs) 2 and 4 was examined using TLR ‐neutralizing antibodies, and activation of extracellular signal‐regulated kinase ( ERK) 1/2 and nuclear factor‐kappa B ( NF ‐ κ B) p65 were measured by western blotting and ELISA , respectively. Eikenella corrodens ‐ LPS increased secretion of interleukin‐8 ( IL ‐8), monocyte chemotactic protein 1 ( MCP ‐1), and granulocyte–macrophage colony‐stimulating factor ( GM ‐ CSF), and expression of ICAM ‐1 on the surface of HCAEC s, consistent with the increased adhesion of THP ‐1 cells. Moreover, E. corrodens ‐ LPS interacted with TLR 4, a key receptor able to maintain the levels of IL ‐8, MCP ‐1, and GM ‐ CSF in HCAEC s. Phosphorylation of ERK 1/2 and activation of NF ‐ κ B p65 were also increased. The results indicate that E. corrodens‐ LPS activates HCAEC s through TLR 4, ERK, and NF ‐ κ B p65, triggering a pro‐atherosclerotic endothelial response and enhancing monocyte adhesion.