Chronic bacterial infection caused by Staphylococcus aureus does not promote atherosclerotic progression in hyperlipidemic mice

Rupture of atherosclerotic plaques can generate thrombi that occlude blood flow and cause acute myocardial infarction (AMI) and acute ischemic stroke (AIS) that are leading causes of death and disability. Patients that develop severe bacterial infections are at increased risk of AMI and AIS, but the mechanisms underlying this association have not been well-characterized.

Previous studies have reported that low-density lipoprotein (LDL) carries bacterial small (s)RNAs that can influence macrophage polarization within plaques, but whether infection alters LDL-associated sRNA or atherosclerotic plaque characteristics to promote AMI/AIS is unclear. Here, we tested whether chronic infection by the Gram-positive pathobiont Staphylococcus aureus was sufficient to alter LDL-associated bacterial sRNA and promote pathogenic changes in atheromatous plaques.