Accelerates Atherosclerosis Macrophage-Driven Aberrant Proinflammatory Response and Lipid Metabolism.

Periodontitis, an oral chronic inflammatory disease, is reported to show an association with atherosclerotic vascular disease. is an oral commensal bacterium that is abundantly implicated in various forms of periodontal diseases; however, its role in the pathogenesis of atherosclerosis is unclear. This study aimed to elucidate the underlying pathogenic mechanisms of atherosclerosis induced by to provide new insight on the prevention and treatment of atherosclerosis. We used an animal model, that is, ApoE mice were infected with by oral gavage, and co-culture models to assess the pathogenicity of The results indicate that ATCC 25586 invaded aortic tissues and substantially increased the progression of atherosclerotic lesions. In addition, changed plaque composition into a less-stable phenotype, characterized with increased subcutaneous macrophage infiltration, M1 polarization, lipid deposition, cell apoptosis, and reduced extracellular matrix and collagen content. The serum levels of pro-atherosclerotic factors, such as interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, monocyte chemoattractant protein-1 (MCP-1), c-reactive protein, and oxidized low-density lipoprotein (ox-LDL) and microRNAs (miR-146a, miR-155, and miR-23b) were considerably increased after stimulation, whereas HDL-c level was reduced. induced macrophage apoptosis in a time- and dose-dependent manner. facilitated ox-LDL-induced cholesterol phagocytosis and accumulation by regulating the expression of lipid metabolism-related genes (AR-A1, ACAT1, ABCA1, and ABCG1). further worsened the atherosclerotic plaque microenvironment by considerably increasing the levels of IL-6; IL-1β; TNF-α; MCP-1; and MMP-2, 8, and 9 and by suppressing fibronectin (FN) 1 levels during foam cell formation. This study shows that ATCC 25586 is implicated in atherosclerosis by causing aberrant activation and lipid metabolism in macrophage.