Increased Atherogenesis during Streptococcus mutans Infection in ApoE-null Mice

Abstract

A supplemental appendix to this article is published electronically only at http://jdr.sagepub.com/supplemental. 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.

Polymicrobial Infection with Major Periodontal Pathogens Induced Periodontal Disease and Aortic Atherosclerosis in Hyperlipidemic ApoEnull Mice

“…Briefly, proatherogenic ApoE null mice were used as a model for atherosclerosis [35], [36] and to examine the role of oral pathogen in induction of atherosclerosis [24], [25]. Male ApoE −/− B6.129P2- Apoe tm1Unc /J mice, eight-weeks-old (The Jackson Laboratories, Bar Harbor, ME) were kept in groups and housed in microisolator plastic cages.…”

Identification of a Supramolecular Functional Architecture of Streptococcus mutans Adhesin P1 on the Bacterial Cell Surface

“…This ubiquitous infectious disease affects developed as well as non-developed countries with annual costs estimated by the American Dental Association to total over $40 billion annually in the United States alone. Additionally, S. mutans has been identified as a causative agent of infectious endocarditis (2)(3)(4)(5). Identifying how S. mutans interacts with host components at the molecular level is essential for a comprehensive understanding of the virulence properties of the organism.…”

The Collagen Binding Protein Cnm Contributes to Oral Colonization and Cariogenicity of Streptococcus mutans OMZ175

“…Previously, we showed that Cnm mediates the invasion of human coronary artery endothelial cells (HCAEC) in vitro and that Cnm ϩ strains exhibit increased virulence in the Galleria mellonella insect model (26). Moreover, recent investigation of S. mutans collagen-binding proteins (CBPs), such as Cnm and Cbm, has linked these adhesins with extraoral infections, including infective endocarditis, hemorrhagic stroke, and atherosclerotic plaque development (1,(27)(28)(29). To date, studies have focused on the role of Cnm in the extraoral virulence of S. mutans but have yet to elucidate whether Cnm confers any advantage on S. mutans in the colonization of oral tissues and the development of dental caries.…”