A new study in the Journal of the American Heart Association has found that viridans group streptococci – bacteria commonly present in the mouth – are often located inside atherosclerotic plaques and may play a role in plaque rupture through biofilm formation and immune activation.
Researchers studied coronary plaques from 121 autopsies of sudden deaths and plaque tissue from 96 surgical endarterectomy patients. They used polymerase chain reaction (qPCR), immunohistochemistry, and gene expression analysis to look for bacterial DNA and to evaluate immune signaling. Laboratory experiments were also performed to test immune responses to the bacteria.
Bacterial DNA was found in about two-thirds of the plaque samples, with viridansstreptococci being the most common type detected, appearing in around 42 percent of cases. Microscopy confirmed that these bacteria were present as biofilms inside the lipid core of advanced plaques. In this form, the bacteria were not recognized by macrophages, suggesting they can persist without detection by the immune system.
In samples with plaque rupture or thrombosis, however, streptococci were found outside the biofilm, inside the fibrous cap, and close to immune cells. These dispersed bacteria were associated with activation of toll-like receptor 2 (TLR2) pathways and NF-κB signaling, which trigger both innate and adaptive immune responses.
Gene expression studies supported these findings, showing that plaques containing streptococcal DNA had higher activity in immune recognition pathways, particularly those involving TLR2, TLR6, and TLR4.
The study also noted that streptococcal immunopositivity was linked with more severe atherosclerosis and with deaths due to coronary heart disease or myocardial infarction. Nearly 90 percent of advanced lesions and ruptured plaques tested positive for the bacteria compared with far fewer early-stage plaques.
According to the authors, these results suggest that bacterial biofilms may remain hidden in plaques until bacteria are released, at which point they can activate inflammation and contribute to plaque instability. The findings point to a possible role for bacterial detection in assessing plaque vulnerability. Methods such as bacterial immunohistochemistry and qPCR could provide new tools for analyzing atherosclerotic tissue, though clinical validation is required before they could be applied in practice.
The authors conclude that chronic bacterial biofilms may be an underrecognized factor in transforming stable plaques into rupture-prone lesions. Further research will be needed to determine whether bacterial detection could aid in risk stratification or whether therapies targeting biofilms could help in prevention.
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