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Figure 1. Models linking mechanisms governing pathogen-accelerated atherosclerosis. Four putative mechanisms by which infection may contribute to accelerated atherosclerosis include the following: (1) direct microbial invasion of vascular endothelium, whereby these infected cells would become immunologically activated in a manner that would set into motion events that would lead to the deposition of atheroma (detailed in Fig. 2); (2) immunological sounding, in which the host response to an extravascular infection leads to seeding of cytokines and chemokines into the circulation, with subsequent activation of vascular endothelium (detailed in Fig. 3); (3) pathogen trafficking, whereby pathogens are shuttled from a site of infection inside inflammatory cells to activated endothelium to gain access to this site (detailed in Fig. 4); and (4) auto-immune reaction, whereby bacterial molecules elicit a specific antibody that is cross-reactive with host molecules (detailed in Fig. 5). These pathways can occur alone or concurrently, and may not necessarily be mutually exclusive.
