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J Dent Res. 2012 Mar;91(3):255-60. doi: 10.1177/0022034511435101. Epub 2012 Jan 18.

Increased atherogenesis during Streptococcus mutans infection in ApoE-null mice.

Author information

1
Department of Periodontology, University of Florida, Gainesville, FL 32610-0424, USA. kesavalu@dental.ufl.edu

Abstract

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 (ApoE(null)) mice without and with balloon angioplasty (BA) injury, a model of restenosis. ApoE(null) 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.

PMID:
22262633
PMCID:
PMC3275337
DOI:
10.1177/0022034511435101
[Indexed for MEDLINE]
Free PMC Article

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