PT  - JOURNAL ARTICLE
AU  - T W Weiss
AU  - H Kvakan
AU  - C Kaun
AU  - M Prager
AU  - W S Speidl
AU  - G Zorn
AU  - S Pfaffenberger
AU  - I Huk
AU  - G Maurer
AU  - K Huber
AU  - J Wojta
TI  - No evidence for a direct role of <em>Helicobacter pylori</em> and <em>Mycoplasma pneumoniae</em> in carotid artery atherosclerosis
AID  - 10.1136/jcp.2005.034314
DP  - 2006 Nov 01
TA  - Journal of Clinical Pathology
PG  - 1186--1190
VI  - 59
IP  - 11
4099  - http://jcp.bmj.com/content/59/11/1186.short
4100  - http://jcp.bmj.com/content/59/11/1186.full
SO  - J Clin Pathol2006 Nov 01; 59
AB  - Background: That infections with certain pathogens, by initiating an inflammatory response, may contribute to the development of atherosclerosis is suggested by clinical and experimental evidence. Aim: To analyse atherosclerotic plaques of the carotid artery, samples of apparently healthy greater saphenous veins and circulating leucocytes from the same individual patients for the presence of Helicobacter pylori and Mycoplasma pneumoniae. Methods: Samples from 36 patients undergoing carotid endarterectomy for symptomatic carotid artery stenosis were analysed by polymerase chain reaction for the presence of DNA specific for H pylori and M pneumoniae. IgG antibody titres against H pylori and M pneumoniae and plasma levels of soluble E-selectin, soluble intercellular adhesion molecule-1 and soluble vascular cell adhesion molecule-1 were determined. Results:M pneumoniae-specific DNA was detected in the atherosclerotic plaques of 13 of 36 (36.1%) patients, in the saphenous veins of 9 of 36 (25%) patients and in the leucocytes of 27 of 36 (75%) patients. No salient association was observed between the presence of M pneumoniae-specific DNA in leucocytes and atherosclerotic plaques or veins. A marked correlation between the presence of M pneumoniae in the respective specimens and the studied inflammatory markers or the presence of anti-M pneumoniae antibodies was not observed. 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 with symptomatic carotid artery stenosis do not support a role for these pathogens in the development of atherosclerosis due to a direct interaction of the bacteria with the vasculature.