Department of Periodontology, University of Florida, Gainesville, FL 32610-0424, USA.
J Dent Res. 2012 Mar;91(3):255-60. doi: 10.1177/0022034511435101. Epub 2012 Jan 18.
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.
变形链球菌是一种龋齿病原体，也会引起心内膜炎，并在动脉粥样硬化斑块中被检测到。我们研究了侵袭性变形链球菌 OMZ175 菌株在载脂蛋白 E 缺陷（ApoE(null)）小鼠中是否具有促进斑块生长的潜力，这些小鼠未接受和接受球囊血管成形术（BA）损伤，这是一种再狭窄模型。将 ApoE(null) 小鼠分为 4 组（N = 10），每组 2 组接受和不接受 BA。BA 和非 BA 组各有一组感染变形链球菌（Sm）。在感染后 6-20 周测量 Sm 感染的 ApoE(null)小鼠的 S. mutans DNA、斑块面积、炎症细胞浸润和 Toll 样受体（TLR）表达。在主动脉、肝脏、脾脏和心脏中检测到 S. mutans 基因组 DNA。在接受 BA（Sm+BA）感染的感染小鼠中，斑块生长明显高于未感染组（p < 0.03）。在未接受 BA 感染的情况下（Sm），斑块大小增加，但没有达到显著水平。来自 Sm 和 Sm+BA 组的主动脉标本显示巨噬细胞数量增加，BA 小鼠的 TLR4 表达增加。总之，变形链球菌感染加速了血管成形术后的斑块生长、巨噬细胞浸润和 TLR4 表达。变形链球菌也可能与未受伤动脉的动脉粥样硬化斑块生长有关。
