title: No evidence for a direct role of Helicobacter pylori and Mycoplasma pneumoniae in carotid artery atherosclerosis.
abstract: 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.
  
  
  OBJECTIVE
  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.
authors.affiliation: The Ludwig Boltzmann Foundation for Cardiovascular Research, Vienna, Austria.
authors.forename: T W
authors.initials: TW
authors.lastname: Weiss
authors.forename: H
authors.initials: H
authors.lastname: Kvakan
authors.forename: C
authors.initials: C
authors.lastname: Kaun
authors.forename: M
authors.initials: M
authors.lastname: Prager
authors.forename: W S
authors.initials: WS
authors.lastname: Speidl
authors.forename: G
authors.initials: G
authors.lastname: Zorn
authors.forename: S
authors.initials: S
authors.lastname: Pfaffenberger
authors.forename: I
authors.initials: I
authors.lastname: Huk
authors.forename: G
authors.initials: G
authors.lastname: Maurer
authors.forename: K
authors.initials: K
authors.lastname: Huber
authors.forename: J
authors.initials: J
authors.lastname: Wojta
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D050197:Atherosclerosis / Q000382:microbiology* / Q000601:surgery; D002340:Carotid Artery Diseases / Q000382:microbiology* / Q000601:surgery; D015815:Cell Adhesion Molecules / Q000097:blood; D004269:DNA, Bacterial / Q000032:analysis; D005260:Female; D016481:Helicobacter Infections / Q000150:complications; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D007962:Leukocytes / Q000382:microbiology; D008297:Male; D008875:Middle Aged; D009175:Mycoplasma Infections / Q000150:complications; D009177:Mycoplasma pneumoniae / Q000302:isolation & purification*; D016133:Polymerase Chain Reaction / Q000379:methods; D012501:Saphenous Vein / Q000382:microbiology
chemical_list: D015815:Cell Adhesion Molecules; D004269:DNA, Bacterial; D018836:Inflammation Mediators