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(Circulation Research. 2008;102:861.)
© 2008 American Heart Association, Inc.

Editorials

Chlamydophila pneumoniae and Endothelial Activation

The Smoke That Precedes the Fire of Atherosclerosis?

Sean P. Didion

From the Department of Internal Medicine, Division of Cardiovascular Medicine, The University of Iowa Carver College of Medicine, Iowa City.

Correspondence to Sean P. Didion, PhD, Department of Internal Medicine, Division of Cardiovascular Medicine, The University of Iowa Carver College of Medicine, 340-G Eckstein Medical Research Building, Iowa City, IA 52242. E-mail sean-didion@uiowa.edu

See related article, pages 888–895

Key Words: atherosclerosis • endothelium • cytokines • infection • inflammation

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Exactly 100 years ago, the physician Sir William Osler suggested an important role for inflammation, as well as infection, in the pathogenesis of atherosclerosis.¹ Indeed, it is now well accepted that atherosclerosis is a disease with a large inflammatory component.² In addition to traditional risk factors, such as hypertension, hyperlipidemia, diabetes, and smoking, previous, as well as chronic or recurrent, infection has emerged as a novel risk factor for atherosclerosis. Cytomegalovirus, herpes simplex virus, Helicobacter pylori, and hepatitis A are a few examples of pathogenic agents that have been, in 1 form or another, associated with atherosclerosis.³ However, no association appears to have garnered more attention, or plausibility, than that between Chlamydophila pneumoniae (formerly Chlamydia pneumonia) infection and atherosclerosis.

C pneumoniae is an obligate intracellular and Gram-negative bacterium and is primarily a pathogen of the respiratory system. Based on serological studies, the prevalence of C pneumoniae, has been estimated to be 50% in young to middle-aged adults and can reach as high as 70% with advanced age,⁴ suggesting that C pneumoniae exposure is not only common but is also recurrent during one’s lifetime. C pneumoniae accounts for nearly 10% of all community-acquired bacterial pneumonias and is categorized among the "atypical pneumonias," including that caused by Mycoplasma pneumoniae and Legionella pneumophila, and is capable of causing chronic as well as subclinical infection.^3,5

The first evidence linking C pneumoniae infection and atherosclerosis was obtained from the finding that individuals with coronary heart disease and acute myocardial infarction were . . . [Full Text of this Article]

Related Article:

Simvastatin Reduces Chlamydophila pneumoniae–Mediated Histone Modifications and Gene Expression in Cultured Human Endothelial Cells

Bernd Schmeck, Wiebke Beermann, Philippe Dje N’Guessan, Andreas C. Hocke, Bastian Opitz, Julia Eitel, Quoc Thai Dinh, Martin Witzenrath, Matthias Krüll, Norbert Suttorp, and Stefan Hippenstiel
Circ. Res. 2008 102: 888-895. [Abstract] [Full Text] [PDF]