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Infection and Immunity, February 2006, p. 1376-1380, Vol. 74, No. 2
0019-9567/06/$08.00+0 doi:10.1128/IAI.74.2.1376-1380.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Department of General Dentistry, Goldman School of Dental Medicine, Boston University, Boston, Massachusetts 02118,1 Department of Dental Public Health, Nihon University School of Dentistry at Matsudo, Chiba 271-8587, Japan,2 Department of Medicine, Section of Infectious Diseases, Boston University School of Medicine, Boston, Massachusetts 02118,3 Department of Conservative Dentistry, Tokushima University School of Dentistry, Tokushima 770-8504, Japan,4 Department of Oral Microbiology, Kanagawa Dental College, Yokosuka, Kanagawa 238-8580, Japan,5 Department of Periodontology and Oral Biology, Goldman School of Dental Medicine, Boston University, Boston, Massachusetts 02118,6 Department of Microbiology, Boston University School of Medicine, Boston, Massachusetts 021187
Received 13 June 2005/ Returned for modification 29 August 2005/ Accepted 2 November 2005
Here we report on early inflammatory events associated with Porphyromonas gingivalis-accelerated atherosclerosis in apolipoprotein E knockout (ApoE/) mice. Animals challenged with P. gingivalis presented with increased macrophage infiltration, innate immune marker expression, and atheroma without elevated systemic inflammatory mediators. This early local inflammatory response was prevented in mice immunized with P. gingivalis. We conclude that localized up-regulation of innate immune markers early after infection, rather than systemic inflammation, contributes to pathogen-accelerated atherosclerosis.
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