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Synopsis

Potential Infectious Etiologies of Atherosclerosis: A Multifactorial Perspective

Siobhán O'Connor,* Christopher Taylor,† Lee Ann Campbell,‡ Stephen Epstein,§ and Peter Libby¶
*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; and ¶Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA

Figure 2. Possible direct effects of Chlamydia pneumoniae (Cpn) on atheromata. Cpn infection augments endothelial cell production of inflammatory cytokines and expression of adhesion molecules, e.g., vascular cell adhesion molecule (VCAM)-1, enhancing leukocyte recruitment to the arterial wall. Chlamydial endotoxin (LPS) may promote macrophage foam cell formation at the site. Chlamydial heat shock protein (HSP-60) may elicit proinflammatory functions from arterial wall macrophages, endothelium, and smooth muscle cells (SMC), or promote macrophage oxidation of lipoproteins.

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Figure 2. Possible direct effects of Chlamydia pneumoniae (Cpn) on atheromata. Cpn infection augments endothelial cell production of inflammatory cytokines and expression of adhesion molecules, e.g., vascular cell adhesion molecule (VCAM)-1, enhancing leukocyte recruitment to the arterial wall. Chlamydial endotoxin (LPS) may promote macrophage foam cell formation at the site. Chlamydial heat shock protein (HSP-60) may elicit proinflammatory functions from arterial wall macrophages, endothelium, and smooth muscle cells (SMC), or promote macrophage oxidation of lipoproteins.
 


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This page last reviewed December 08, 2001

Emerging Infectious Diseases Journal
National Center for Infectious Diseases
Centers for Disease Control and Prevention