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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 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

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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