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The most recent version of this article was published on 1 November 2006

J Clin Pathol. Published Online First: 27 April 2006. doi:10.1136/jcp.2005.034314
Copyright © 2006 by the BMJ Publishing Group Ltd & Association of Clinical Pathologists.

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*Carotid Artery Disease

Microbiology

No evidence for a direct role of helicobacter pylori and mycoplasma pneumoniae in carotid artery atherosclerosis based on their respective presence in the atherosclerotic plaque, in healthy vessels and in circulating leukocytes from the same individuals

Thomas W Weiss 1, Heda Kvakan 1, Christoph Kaun 1, Manfred Prager 1, Walter S Speidl 1, Gerlinde Zorn 1, Stefan Pfaffenberger 1, Ihor Huk 1, Gerald Maurer 1, Kurt Huber 2 and Johann Wojta 1*

1 Medical University of Vienna, Austria
2 Wilheminenhospital Vienna, Austria

* To whom correspondence should be addressed. E-mail: johann.wojta{at}meduniwien.ac.at.

Accepted 23 February 2006


*   Abstract

Aims: Clinical and experimental evidence suggests that infections with certain pathogens by initiating an inflammatory response might contribute to the development of atherosclerosis. We analysed atherosclerotic plaques of the carotid artery, samples of apparently healthy greater saphenous veins, and circulating leukocytes from the same individual patients for the presence of Helicobacter pylori and Mycoplasma pneumoniae.

Methods: From 36 patients undergoing carotid endarterectomy for symptomatic carotid artery stenosis, these samples were analysed by polymerase chain reaction for the presence of H. pylori- and M. pneumoniae-specific DNA. We determined IgG antibody titres against H. pylori and M. pneumoniae and plasma levels of sE-selectin, sICAM-1, and sVCAM-1.

Results: M. pneumoniae-specific DNA was detected in the atherosclerotic plaques of 13 of 36 patients (36.1%) in the saphenous veins of 9 of 36 patients (25%) and in leukocytes of 27 of 36 patients (75%). No significant association between the presence of M. pneumoniae-specific DNA in leukocytes and atherosclerotic plaques or veins was observed. We could not observe a significant correlation between presence of M. pneumoniae in the respective specimens and the studied inflammatory markers or the presence of anti-M. pneumoniae antibodies. H. pylori-specific DNA could not be detected in the specimens tested.

Conclusions: The absence of H. pylori and the random distribution of M. pneumoniae in tissue samples obtained from patients suffering from symptomatic carotid artery stenosis do not support a role of these pathogens in the development of atherosclerosis due to a direct interaction of the bacteria with the vasculature.

Key Words: Atherosclerosis, Carotid artery, Helicobacter pylori, Mycoplasma pneumoniae




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Microbial pathogens and atherosclerosis
Kenneth A Hoekstra, PhD
JCP Online, 1 Dec 2006 [Full text]



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Copyright © 2006 by the BMJ Publishing Group Ltd & Association of Clinical Pathologists.