Porphyromonas gingivalis stimulates monocyte adhesion to human umbilical vein endothelial cells.

Monocyte recruitment to the endothelium is a crucial step in the inflammatory response that precedes the development of atherosclerosis. We assessed the effect of Porphyromonas gingivalis on monocyte adhesion to endothelial cells, cytokine production during monocyte/endothelial cell co-culture, and the expression of cell adhesion molecules on human umbilical vein endothelial cells (HUVEC) and their ligands on monocytes. Porphyromonas gingivalis challenge significantly increased the adhesion of THP-1 monocytes to HUVEC, the production of interleukin (IL)-6, IL-8, and monocyte chemoattractant protein 1 (MCP-1) in co-cultures of HUVEC and THP-1 cells, and the transcription and translation of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin in HUVEC. The transcription of tumor necrosis factor receptor-associated factor 1 was also increased in HUVEC and THP-1 cells by P. gingivalis infection. Moreover, the stimulation of monocyte adhesion to HUVEC by P. gingivalis infection was partially inhibited by pretreatment with a mixture of anti-ICAM-1, -VCAM, and -E-selectin monoclonal antibodies. These data suggest that adherence between HUVEC and THP-1 cells, followed by the production of cytokines and chemokines, was enhanced by increased expression of cell adhesion molecules on P. gingivalis-sensitized HUVEC, which in turn led to inflammatory atherogenesis.