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Volume 7, Number 5—October 2001
Synopsis

Potential Infectious Etiologies of Atherosclerosis: A Multifactorial Perspective

Siobhán O'Connor*Comments to Author , Christopher Taylor†, Lee Ann Campbell‡, Stephen Epstein§, and Peter Libby¶
Author affiliations: *Centers for Disease Control and Prevention, Atlanta, GA, USA; †National Institute for Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA; ‡University of Washington, Seattle, Washington, USA; §MedStar Research Institute, Washington Hospital Center, Washington, DC, USA; ¶Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA

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Figure 1

"Echo" hypothesis: activation of atheroma-associated cells by bacterial products and cytokines released in response to extravascular infection. a. Extravascular infection stimulates production of inflammatory cytokines, e.g. interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α), that can elicit an echo cytokine response from inflammatory cells in residence at sites of atherogenesis. Circulating microbial products, e.g. endotoxin, can also elicit an echo response at the artery wall. b. Ext

Figure 1. . "Echo" hypothesis: activation of atheroma-associated cells by bacterial products and cytokines released in response to extravascular infection. a. Extravascular infection stimulates production of inflammatory cytokines, e.g. interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α), that can elicit an echo cytokine response from inflammatory cells in residence at sites of atherogenesis. Circulating microbial products, e.g. endotoxin, can also elicit an echo response at the artery wall. b. Extravascular infection-elicited cytokines stimulate hepatic synthesis of acute-phase reactants. Some factors, e.g. fibrinogen, might influence complicated atheromata formation or arterial thrombosis.

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