Increased atherogenesis during Streptococcus mutans infection in ApoE-null mice

Area of Science:

• Microbiology
• Cardiovascular Research
• Immunology

Background:

• Streptococcus mutans is linked to dental caries, endocarditis, and atherosclerosis.
• An invasive strain, OMZ175, was examined for its role in plaque formation.
• Apolipoprotein E deficient (ApoE(null)) mice with balloon angioplasty (BA) served as a restenosis model.

Purpose of the Study:

• To investigate the effect of S. mutans infection on plaque growth in ApoE(null) mice.
• To assess S. mutans' impact with and without BA-induced injury.
• To analyze inflammatory responses and Toll-like receptor (TLR) expression.

Main Methods:

• ApoE(null) mice were divided into four groups: S. mutans infected with BA (Sm+BA), non-infected with BA, S. mutans infected without BA (Sm), and non-infected without BA.
• Mice were monitored for 6-20 weeks post-infection.
• S. mutans DNA, plaque area, macrophage infiltration, and TLR expression were quantified.

Main Results:

• S. mutans DNA was detected systemically (aorta, liver, spleen, heart).
• Significantly increased plaque growth was observed in the Sm+BA group compared to controls (p < 0.03).
• Increased macrophage infiltration and TLR4 expression were noted in infected mice, particularly in the BA group.

Conclusions:

• S. mutans infection exacerbates plaque growth, macrophage invasion, and TLR4 expression following angioplasty.
• The findings suggest a potential role for S. mutans in accelerating atherosclerotic plaque development, even in non-injured arteries.