Extended exposure of lipopolysaccharide fraction from Porphyromonas gingivalis facilitates mononuclear cell adhesion to vascular endothelium via Toll-like receptor-2 dependent mechanism

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 Pg. 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 Pg.-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 Pg.-LPS fraction peaked after 24 h of incubation, whereas those treated with E. coli-LPS fraction maximized after 4 h of incubation. A fluorescent immunobinding assay revealed that Pg.-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 Pg.-LPS fraction-facilitated mononuclear cell adhesion to HUVECs. In conclusion, these results suggest that chronic Pg. 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 Pg.-LPS signal transduction. (C) 2007 Elsevier Ireland Ltd. All rights reserved.