Immune activation as effect modifier of atherogenesis in chronic infection

Although no study has proven that infections cause atherosclerotic disease, findings suggest that exposure to infections such as Chlamydia pneumoniae, Helicobacter pylori, and bacterial infections related to periodontal disease or smoking might influence the development of heart, carotid, and peripheral vascular disease. Epidemiological data convincingly demonstrate risk for atherosclerotic disease associated with bacterial infection and endotoxemia; however, the independent contributions to disease and pathogenic mechanisms of endotoxin remained elusive. Investigation into this relation tested the correlation between endotoxin and neopterin. Data indicated that neopterin, which reflects immune activation of monocytes/macrophages, functions as atherogenic effect modifying factor on the effects of endotoxin. We hypothesize that immune activation via induction of endotoxin hyperresponsiveness determines the atherogenic potential of Gram-negative infections.