0
We're unable to sign you in at this time. Please try again in a few minutes.
Retry
We were able to sign you in, but your subscription(s) could not be found. Please try again in a few minutes.
Retry
There may be a problem with your account. Please contact the AMA Service Center to resolve this issue.
Contact the AMA Service Center:
Telephone: 1 (800) 262-2350 or 1 (312) 670-7827  *   Email: subscriptions@jamanetwork.com
Error Message ......
Special Communication |

Chlamydia pneumoniae as an Emerging Risk Factor in Cardiovascular Disease

Murat V. Kalayoglu, MD, PhD; Peter Libby, MD; Gerald I. Byrne, PhD
JAMA. 2002;288(21):2724-2731. doi:10.1001/jama.288.21.2724.
Text Size: A A A
Published online

Recent appreciation of atherosclerosis as a chronic, inflammatory disease has rekindled efforts to examine the role that infectious agents may play in atherogenesis. In particular, much interest has focused on infection with Chlamydia pneumoniae. The possibility that a prokaryote contributes to atherogenesis has high clinical interest, as C pneumoniae infection may be a treatable risk factor. To review the evidence implicating C pneumoniae in the pathogenesis of atherosclerosis, we searched MEDLINE for articles published between January 1966 and October 2002 on the association of C pneumoniae and atherosclerosis. We also used online resources, texts, meeting abstracts, and expert opinion. We included 5 types of studies (epidemiological, pathology based, animal model, cell biology, and human antibiotic treatment trials) and extracted diagnostic, pathophysiologic, and therapeutic information from the selected literature; consensus was reached on interpretation discrepancies. Chlamydia pneumoniae is associated with atherosclerosis by epidemiological and pathology-based studies. Animal model and cell biology studies suggest that the pathogen can modulate atheroma biology, including lipid- and inflammatory-related processes. Although some preliminary antibiotic treatment trials in patients with coronary artery disease indicated a reduction in recurrent coronary events, larger studies have not shown benefits in individuals with stable coronary artery disease. It is unlikely that C pneumoniae infection is necessary to initiate atherosclerosis. Furthermore, conventional antibiotic therapy may not eradicate the organism or reduce mortality in individuals with atherosclerotic vascular disease. Nevertheless, the current body of evidence establishes this pathogen as a plausible, potentially modifiable risk factor in cardiovascular disease.

Figures in this Article

Sign in

Create a free personal account to sign up for alerts, share articles, and more.

Purchase Options

• Buy this article
• Subscribe to the journal

Figures

Figure 1. Life Cycle of Chlamydia pneumoniae
Graphic Jump Location
Chlamydial elementary bodies adhere to the host cell and are endocytosed (1). The pathogen prevents phagosome-lysosome fusion, differentiates into the reticulate body (2), and begins replicating within the inclusion (3). Replicating reticulate bodies may redifferentiate back into elementary bodies (4a and 5) and lyse the host cell to begin a new round of infection (6). In addition, under conditions of immune stress such as the presence of IFN-γ, the pathogen may adopt a noninfectious, nonreplicating persistent form (4b); when the stress is removed, the pathogen can redifferentiate into infectious elementary bodies to begin a new cycle of infection. IFN indicates interferon.
Figure 2. Mechanisms by Which Chlamydia pneumoniae May Promote Atherosclerosis
Graphic Jump Location
Circulating monocytes infected with C pneumoniae adhere to and migrate through the endothelium, undergo cytolysis, release infectious elementary bodies, and establish chronic infection within the intima. Chlamydia pneumoniae in the persistent form, contained within a subgroup of host cells (not shown), reenter the productive life cycle, lyse the cells, and are released as infectious elementary bodies within the intima. Elementary bodies are capable of infecting and replicating within all atheroma cell types, including resident macrophages, smooth muscle cells, and endothelial cells. Chlamydia pneumoniae modulates cell biology to trigger inflammatory cascades, release matrix metalloproteinases and procoagulant factors, recruit specific T-cell responses, alter cellular lipid metabolism, promote smooth muscle cell proliferation, induce endothelial leukocyte adhesion molecule expression, and impair arterial relaxation. VCAM indicates vascular cell adhesion molecule; ICAM, intercellular adhesion molecule; E-selectin, endothelium selectin; IL, interleukin; LDL, low-density lipoprotein; oxLDL, oxidized LDL; cHsp60, chlamydial heat shock protein 60 kd; cLPS, chlamydial lipopolysaccharide; MIP, macrophage inflammatory protein; MCP, monocyte chemoattractant protein; TNF, tumor necrosis factor; IFN, interferon; and FGF, fibroblast growth factor.

Tables

References

CME
Meets CME requirements for:
Browse CME for all U.S. States
Accreditation Information
The American Medical Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The AMA designates this journal-based CME activity for a maximum of 1 AMA PRA Category 1 CreditTM per course. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Physicians who complete the CME course and score at least 80% correct on the quiz are eligible for AMA PRA Category 1 CreditTM.
Note: You must get at least of the answers correct to pass this quiz.
You have not filled in all the answers to complete this quiz
The following questions were not answered:
Sorry, you have unsuccessfully completed this CME quiz with a score of
The following questions were not answered correctly:
Commitment to Change (optional):
Indicate what change(s) you will implement in your practice, if any, based on this CME course.
Your quiz results:
The filled radio buttons indicate your responses. The preferred responses are highlighted
For CME Course: A Proposed Model for Initial Assessment and Management of Acute Heart Failure Syndromes
Indicate what changes(s) you will implement in your practice, if any, based on this CME course.

Multimedia

Some tools below are only available to our subscribers or users with an online account.

Web of Science® Times Cited: 171

Sign in

Create a free personal account to sign up for alerts, share articles, and more.

Purchase Options

• Buy this article
• Subscribe to the journal

Related Content

Customize your page view by dragging & repositioning the boxes below.

Articles Related By Topic
Related Collections
PubMed Articles
Jobs
JAMAevidence.com

Users' Guides to the Medical Literature
Clinical Scenario

Users' Guides to the Medical Literature
In contrast, the authors of the Clopidogrel Versus Aspirin in Patients at Risk of Ischaemic...

brightcove.createExperiences();