ORIGINAL ARTICLE

No evidence for a direct role of Helicobacter pylori and Mycoplasma pneumoniae in carotid artery atherosclerosis

T W Weiss¹, H Kvakan², C Kaun², M Prager³, W S Speidl², G Zorn², S Pfaffenberger², I Huk³, G Maurer², K Huber² and J Wojta¹

¹ The Ludwig Boltzmann Foundation for Cardiovascular Research, Vienna, Austria
² Department of Internal Medicine II, Medical University Vienna, Vienna, Austria
³ Department of Vascular Surgery, Medical University Vienna, Vienna, Austria
⁴ III Medical Department for Cardiology and Emergency Medicine, Wilhelminenspital, Vienna, Austria

Correspondence to:
Correspondence to:
J Wojta
Department of Internal Medicine II, Medical University of Vienna, Waehringer Guertel 18-20, A-1090 Vienna, Austria; johann.wojta{at}meduniwien.ac.at

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.

Abbreviations: CAD, coronary artery disease; CRP, C reactive protein; ELISA, enzyme-linked immunosorbent assay; GSV, greater saphenous vein; PCR, polymerase chain reaction; sE-selectin, soluble E-selectin; sICAM-1, soluble intercellular adhesion molecule-1; sVCAM-1, soluble vascular cell adhesion molecule-1

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