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In this study, we evaluated whether the heat\u2010shock protein GroEL of <jats:italic>Fusobacterium nucleatum<\/jats:italic>, one of the most prevalent bacteria in periodontitis, induces factors that predispose to atherosclerosis in human microvascular endothelial cells (HMEC\u20101) and apolipoprotein E\u2010deficient (ApoE<jats:sup>\u2212\/\u2212<\/jats:sup>) mice. GroEL induced the expression of chemokines such as monocyte chemoattractant protein\u20101 and interleukin\u20108 as well as cell adhesion molecules, such as intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and E\u2010selectin. GroEL induced the activity of tissue factor and reduced the activity of the tissue factor pathway inhibitor. Foam cell formation was induced by GroEL. GroEL\u2010injected ApoE<jats:sup>\u2212\/\u2212<\/jats:sup> mice showed significant atherosclerotic lesion progression compared with control mice. Serum levels of risk factors for atherosclerosis such as interleukin\u20106, C\u2010reactive protein, and low\u2010density lipoprotein were increased in GroEL\u2010injected ApoE<jats:sup>\u2212\/\u2212<\/jats:sup> mice compared with control mice, whereas serum levels of high\u2010density lipoprotein were decreased. We could detect significantly higher levels of anti\u2010<jats:italic>F.\u00a0nucleatum<\/jats:italic> GroEL antibody in serum and <jats:italic>F.\u00a0nucleatum<\/jats:italic> DNA in gingival crevicular fluid from patients with periodontitis than in that from healthy subjects. Our results indicate that the host response to the GroEL of periodontal pathogens like <jats:italic>F.\u00a0nucleatum<\/jats:italic> may be a mechanism involved in atherosclerosis, supporting the association of periodontitis and systemic infection.<\/jats:p>","DOI":"10.1111\/j.2041-1014.2011.00636.x","type":"journal-article","created":{"date-parts":[[2011,12,24]],"date-time":"2011-12-24T23:29:06Z","timestamp":1324769346000},"page":"109-123","source":"Crossref","is-referenced-by-count":60,"title":["<i>Fusobacterium nucleatum<\/i> GroEL induces risk factors of atherosclerosis in human microvascular endothelial cells and ApoE<sup>\u2212\/\u2212<\/sup> 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