Open AccessPorphyromonas gingivalis stimulates monocyte adhesion to human umbilical vein endothelial cells
Author(s) -
Hashizume Tomomi,
KuritaOchiai Tomoko,
Yamamoto Masafumi
Publication year - 2011
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2011.00786.x
Subject(s) - umbilical vein , porphyromonas gingivalis , biology , monocyte , adhesion , microbiology and biotechnology , immunology , bacteroidaceae , human umbilical vein endothelial cell , cell adhesion , bacteria , cell , in vitro , chemistry , biochemistry , genetics , organic chemistry
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.