Pathogen-accelerated atherosclerosis occurs early after exposure and can be prevented via immunization

Infect Immun. 2006 Feb;74(2):1376-80. doi: 10.1128/IAI.74.2.1376-1380.2006.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Aorta, Thoracic / immunology
  • Aorta, Thoracic / pathology
  • Apolipoproteins E / deficiency
  • Apolipoproteins E / genetics
  • Atherosclerosis / microbiology*
  • Atherosclerosis / pathology
  • Atherosclerosis / prevention & control*
  • Bacteroidaceae Infections / complications*
  • Bacteroidaceae Infections / immunology
  • Bacteroidaceae Infections / microbiology
  • Immunity, Innate
  • Immunization*
  • Inflammation / immunology
  • Inflammation / microbiology
  • Inflammation / prevention & control
  • Male
  • Mice
  • Porphyromonas gingivalis / immunology*
  • Porphyromonas gingivalis / pathogenicity
  • Time Factors

Substances

  • Apolipoproteins E