Innate immune recognition of invasive bacteria accelerates atherosclerosis in apolipoprotein E-deficient mice

Frank C. Gibson, Charlie Hong, Hsin Hua Chou, Hiromichi Yumoto, Jiqiu Chen, Egil Lien, Jodie Wong, Caroline Attardo Genco

Research output: Contribution to journalArticlepeer-review

290 Citations (Scopus)


Background - Infectious diseases have emerged as potential risk factors for cardiovascular disease (CVD). Epidemiological studies support a connection between periodontal disease, a chronic inflammatory disease of the supporting tissues of the teeth, and CVD. Methods and Results - To directly test the connection between periodontal disease and atherosclerosis, apoE-/- mice were orally challenged with the periodontal disease pathogen Porphyromonas gingivalis or an invasion-impaired P gingivalis fimbriae-deficient mutant (FimA-). Both wild-type P gingivalis and the FimA- mutant were detected in blood and aortic arch tissue of apoE-/- mice by PCR after challenge. ApoE-/- mice challenged with wild-type P gingivalis presented with increased atherosclerotic plaque and expressed the innate immune response markers Toll-like receptor (TLR)-2 and TLR-4 in aortic tissue. Despite detection of the FimA- mutant in the blood and in aortic arch tissue, apoE -/- mice challenged with the FimA- mutant did not present with periodontal disease, upregulation of TLRs, or accelerated atherosclerosis. Furthermore, we demonstrate that immunization to control P gingivalis-elicited periodontal disease concomitantly prevents P gingivalis-accelerated atherosclerosis. Conclusions - We conclude that invasive P gingivalis accelerates atherosclerosis.

Original languageEnglish
Pages (from-to)2801-2806
Number of pages6
Issue number22
Publication statusPublished - Jun 8 2004


  • Atherosclerosis
  • Endothelium
  • Infection
  • Inflammation
  • Receptors

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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