Increased atherogenesis during Streptococcus mutans infection in ApoE-null mice

L. Kesavalu, A. R. Lucas, R. K. Verma, L. Liu, E. Dai, E. Sampson, A. Progulske-Fox

Research output: Contribution to journalArticlepeer-review

56 Scopus citations


Streptococcus mutans, a dental caries pathogen, also causes endocarditis and is detected in atheroscelerotic plaque. We investigated the potential for an invasive strain of S. mutans, OMZ175, to accelerate plaque growth in apolipoprotein E deficient (ApoEnull) mice without and with balloon angioplasty (BA) injury, a model of restenosis. ApoEnull mice were divided into 4 groups (N = 10), 2 with and 2 without BA. One each of the BA and non-BA groups was infected with S. mutans (Sm). S. mutans DNA, plaque area, inflammatory cell invasion, and Toll-like receptor (TLR) expression were measured at 6-20 weeks post-infection. S. mutans genomic DNA was detected in the aorta, liver, spleen, and heart. Plaque growth was significantly increased in infected mice with BA (Sm+BA) vs. those in the non-infected groups (p < 0.03). Plaque size was increased after infection without BA (Sm), but did not reach significance. Aortic specimens from both S. mutans and Sm+BA groups displayed increased numbers of macrophages, and TLR4 expression was increased in BA mice. In conclusion, S. mutans infection accelerated plaque growth, macrophage invasion, and TLR4 expression after angioplasty. S. mutans may also be associated with atherosclerotic plaque growth in non-injured arteries.

Original languageEnglish (US)
Pages (from-to)255-260
Number of pages6
JournalJournal of Dental Research
Issue number3
StatePublished - Mar 2012
Externally publishedYes


  • Streptococcus mutans
  • Toll-like receptor 4
  • antibody response
  • atherosclerosis
  • balloon angioplasty
  • macrophage invasion

ASJC Scopus subject areas

  • Dentistry(all)


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