Based on these observations, it may be reasonable to speculate that in the pathogenesis of atherosclerosis associated with bacterial infection, LPS promotes the early stages of pathogenesis by increasing cytokines/chemokines (TNF-α, IL-1β, IL-6, and MCP-1) and the adhesion molecules (VCAM-1 and ICAM-1) of monocytes and ECs, thereby enhancing the recruitment and adhesion of monocytes to those ECs in which the TLR-mediated LPS recognition and activation of cellular signaling may be involved. This evidence concerns the gene CCL2 and atherosclerosis.