There is some evidence that endotoxin-containing bacteria may contribute to atherogenesis. The degree to which bacterial insults contribute to the total body burden of atherosclerotic lesions cannot be determined at this time. It is important to realize that there are other potential sources of injury to the vascular endothelium, mechanical, chemical, immunologic and biological, which may initiate formation of an atherosclerotic plaque. It must also be remembered that the process of atherogenesis is extremely complex and involves many factors other than the initial injury to endothelium. The suggested role for endotoxin, particularly endotoxin from degrading bacteria in macrophages, in concert with the inflammatory factors induced by endotoxin from endothelium and vascular smooth muscle cells, is an attractive hypothesis for several reasons. First, dampening of inflammatory responses by effects of N-3 polyunsaturated fatty acids (omega-3s) is explained, particularly their direct influence on monocyte functions. Second, the hypothesis provides a model system in which the first step in atherogenesis may be studied prospectively, while other factors may be varied to determine their influences on later stages in the process of plaque formation. Recombinant DNA techniques and sophisticated immunologic tools are available to study the entire process, as are animal models in which to conduct studies with relevance to the human. Although at present, the link between foodborne gram-negative bacterial pathogens and atherosclerosis is largely unproven, the possible role of such organisms warrants more research. Additionally, should the link be firmly established, it would further underscore the importance of food safety in the biological sense.
Urinary Thymidine Dimer as a Marker of Total Body Burden of UV-Inflicted DNA Damage in Humans