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Int. J. Mol. Sci. 2013, 14(7), 15105-15120; doi:10.3390/ijms140715105

Chlamydia pneumoniae Infection in Atherosclerotic Lesion Development through Oxidative Stress: A Brief Overview

Department of Public Health and Infectious Diseases, "Sapienza" University, Rome 00185, Italy
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Received: 31 May 2013 / Revised: 4 July 2013 / Accepted: 10 July 2013 / Published: 19 July 2013
(This article belongs to the Special Issue Oxidative Stress in Cardiovascular Disease)
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Abstract

Chlamydia pneumoniae, an obligate intracellular pathogen, is known as a leading cause of respiratory tract infections and, in the last two decades, has been widely associated with atherosclerosis by seroepidemiological studies, and direct detection of the microorganism within atheroma. C. pneumoniae is presumed to play a role in atherosclerosis for its ability to disseminate via peripheral blood mononuclear cells, to replicate and persist within vascular cells, and for its pro-inflammatory and angiogenic effects. Once inside the vascular tissue, C. pneumoniae infection has been shown to induce the production of reactive oxygen species in all the cells involved in atherosclerotic process such as macrophages, platelets, endothelial cells, and vascular smooth muscle cells, leading to oxidative stress. The aim of this review is to summarize the data linking C. pneumoniae-induced oxidative stress to atherosclerotic lesion development. View Full-Text
Keywords: C. pneumoniae; atherosclerosis; oxidative stress; inflammation C. pneumoniae; atherosclerosis; oxidative stress; inflammation
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Di Pietro, M.; Filardo, S.; De Santis, F.; Sessa, R. Chlamydia pneumoniae Infection in Atherosclerotic Lesion Development through Oxidative Stress: A Brief Overview. Int. J. Mol. Sci. 2013, 14, 15105-15120.

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