Certain infectious pathogens contribute to atherogenesis. Indeed, the strong relationship between periodontal pathogens, such as Porphyromonas gingivalis (P.g.) and coronary heart disease has been demonstrated. We investigated the potential role of P.g. in monocyte-endothelial interaction. Lipopolysaccharide (LPS) fraction was extracted from P.g. cultured under anaerobic conditions and compared to that obtained from an Escherichia coli (E. coli) strain (JM109). Human umbilical vein endothelial cells (HUVECs) were incubated in the presence of P.g.-LPS fraction or E. coli-LPS fraction for various periods and mononuclear cell adhesion assays were conducted under flow. The adhesion of mononuclear cells to HUVECs treated with P.g.-LPS fraction peaked after 24h of incubation, whereas those treated with E. coli-LPS fraction maximized after 4h of incubation. A fluorescent immunobinding assay revealed that P.g.-LPS fraction significantly upregulated ICAM-1 and VCAM-1 in HUVECs. Antibodies against ICAM-1 and Toll-like receptor (TLR)-2, but not TLR-4, attenuated P.g.-LPS fraction-facilitated mononuclear cell adhesion to HUVECs. In conclusion, these results suggest that chronic P.g. infection may facilitate monocyte recruitment to vascular endothelium through sustained upregulation of ICAM-1 and VCAM-1. Our findings provide new evidence that the TLR-2 pathway may contribute to atherogenesis by mediating P.g.-LPS signal transduction.