TY - JOUR
T1 - Increased atherogenesis during Streptococcus mutans infection in ApoE-null mice
AU - Kesavalu, L.
AU - Lucas, A. R.
AU - Verma, R. K.
AU - Liu, L.
AU - Dai, E.
AU - Sampson, E.
AU - Progulske-Fox, A.
N1 - Funding Information:
This project was supported by U24 DE016509 from the NIDCR and by the University of Florida Opportunity Research and UF College of Dentistry seed funds.
PY - 2012/3
Y1 - 2012/3
N2 - 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.
AB - 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.
KW - Streptococcus mutans
KW - Toll-like receptor 4
KW - antibody response
KW - atherosclerosis
KW - balloon angioplasty
KW - macrophage invasion
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U2 - 10.1177/0022034511435101
DO - 10.1177/0022034511435101
M3 - Article
C2 - 22262633
AN - SCOPUS:84863160675
SN - 0022-0345
VL - 91
SP - 255
EP - 260
JO - Journal of Dental Research
JF - Journal of Dental Research
IS - 3
ER -