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Microbiology |
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 |
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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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