The presence of bacteria in APs has been demonstrated thanks to advancements in DNA-sequencing methods ( 35– 38). Also, monocytes in the circulation may function as a “Trojan horse” to deliver bacteria from the circulation to vessel walls and sustain the infection ( 7). In some circumstances, these bacteria can induce chronic infection residing within antigen-presenting cells (APCs), such as dendritic cells (DCs) or macrophages ( 30, 32– 34). Bacteria can infect vessel walls directly, thereby leading to their injury and release of inflammatory factors ( 31). Macrophage depletion also promotes AP stability and induces the regression of established APs ( 24).Īn increasing number of studies have shown that infections (particularly chronic infections) are associated with the development of cardiovascular diseases ( 7– 9, 26– 30). Hence, scholars have explored therapeutic alternatives by depletion of macrophages and inducing macrophage death ( 22, 24, 25). Macrophages play a central part in atherosclerosis development and AP destabilization. Several studies have shown that depletion of macrophages in animals results in dramatic reduction of atherosclerosis progression ( 21– 24). Initially, it was thought that infiltrated macrophages could phagocytose lipid to eliminate fat via scavenger receptors ( 17– 19), but the infiltrated macrophages in turn elicit an inflammatory response that damages vessel walls ( 20). Macrophage-derived foam cells are major players in atherosclerosis pathogenesis ( 15, 16).

In fact, inflammation and macrophage deposition have been observed in atherosclerosis for decades ( 11– 14). Studies have suggested that risk factors may add to early atherosclerotic lesions in human coronary arteries, which may result in macrophage recruitment ( 7, 10).

However, the detailed molecular and biological mechanisms of atherosclerosis are not clear. In general, it is believed that risk factors such as hyperlipidemia, hypertension, obesity, diabetes mellitus, and smoking can contribute to the formation of atherosclerotic plaques (APs) ( 6– 9). Atherosclerosis in humans usually affects the “medium” arteries, human coronary, renal, and carotid arteries ( 5). Plaque formation is a hallmark of atherosclerosis ( 4) and is characterized by deposition of fat, cholesterol and calcium in arterial intima. It may be possible to slow down the progress of atherosclerosis by blocking the interactions between CD209s/CD207 and certain atherosclerosis-involved bacteria with ligand-mimic oligosaccharides.Ĭardiovascular diseases caused by atherosclerosis are leading causes of mortality worldwide ( 1– 3). mirabilis interacts with APs in human coronary arteries via CD209s/CD207. mirabilis than that of control mice during infection-challenging. Finally, the hearts from an atherosclerotic mouse model contained higher numbers of P. These interactions were inhibited by addition of a ligand-mimic oligosaccharide and the coverage of the ligand, as well as by anti-CD209 antibody. mirabilis interacted with fresh and CD209s/CD207-expressing APs cut from human coronary arteries, rather than in healthy and smooth arteries. mirabilis that mediated adherence and phagocytosis by macrophages. In this study, we first demonstrated that CD209/CD207 were also receptors for P. We wondered if Proteus mirabilis (a member of Proteobacteria family) could interact with APs through CD209/CD207. A series of studies suggested that certain Gram-negative bacteria were able to interact with dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin or langerin (CD207), thereby resulting in deposition of CD209s at infection sites.

6Division of Cardiothoracic and Vascular Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Chinaīacterial DNAs are constantly detected in atherosclerotic plaques (APs), suggesting that a combination of chronic infection and inflammation may have roles in AP formation.

5Department of Clinical Laboratory, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan, China.

4Laboratory for Plague Microbiology, State Research Center for Applied Microbiology and Biotechnology, Especially Dangerous Infections Department, Obolensk, Russia.

Centers for Disease Control and Prevention, Atlanta, GA, United States

3Division of Global Health Protection, Center for Global Health, U.S.

2Laboratory of Immunology, Brain Korea 21 FOUR Project for Medical Science, Institute for Immunology and Immunological Diseases, Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, South Korea.

1Department of Clinical Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Anisimov 4, Ziyong Sun 5, Xiang Wei 6* and Tie Chen 1* Ying Xue 1†, Qiao Li 1†, Chae Gyu Park 2, John D.

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