Detection of Helicobacter pylori and Chlamydia pneumoniae DNA in human coronary arteries and evaluation of the results with serologic evidence of inflammation.
OBJECTIVE
Atherosclerosis is pathologically similar to a chronic inflammatory response. Recent reports have suggested that Chlamydia pneumoniae (C. pneumoniae) and Helicobacter pylori (H. pylori) play a role in the pathogenesis of atherosclerosis but this relation has not been confirmed on an inflammatory background.


METHODS
Twenty-nine consecutive patients admitted to Suleyman Demirel University Medical School Cardiovascular Surgery Department, Isparta, Turkey between May 2002 to June 2003 were included in the study and the presence of C. pneumoniae and H. pylori DNA in atherosclerotic plaques of 14 coronary endarterectomy specimens and 15 left internal mammarian artery (LIMA) specimens as control subjects were determined by polymerase chain reaction. Serologic evidence of infection and inflammatory markers were also determined in both groups.


RESULTS
Two C. pneumoniae DNA cases from the plaque group (14.3%) and 4 H. pylori DNA cases; 3 from plaque (21.4%) and one from the LIMA groups (6.7%) were detected. The C-reactive protein (mg/L) were higher in DNA positive samples of C. pneumoniae (66.58) and H. pylori (21.93) compared to DNA negatives of C. pneumoniae (8.49) and H. pylori (10.98), similarly interleukin-6 (U/L) levels were higher in DNA positive samples of C. pneumoniae (42.25) and H. pylori (56.37) compared with DNA negatives of C. pneumoniae (17.52) and H. pylori (13.28), but the differences were not statistically significant. Apolipoprotein B levels were significantly higher in C. pneumoniae immunoglobulin M positive cases (0.844 g/L) compared with negatives (0.661 g/L) (p=0.004).


CONCLUSIONS
Chronic infections modify the serum lipid profile in a way that increases the risk of atherosclerosis. The increased titers of inflammation markers in DNA positive patients support inflammation in atherosclerosis, however, the results should be reproduced in a larger cohort.
Adiloglu
Ali K
AK
Department of Microbiology, Suleyman Demirel University School of Medicine, Isparta, Turkey. aadiloglu@yahoo.com
Ocal
Ahmet
A
Can
Rabia
R
Duver
Harun
H
Yavuz
Turan
T
Aridogan
Buket C
BC
D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D001055:Apolipoproteins B / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D016993:Chlamydophila pneumoniae / Q000235:genetics* / Q000276:immunology; D003324:Coronary Artery Disease / Q000378:metabolism*; D003331:Coronary Vessels / Q000378:metabolism*; D004269:DNA, Bacterial / Q000378:metabolism*; D005260:Female; D016480:Helicobacter pylori / Q000235:genetics* / Q000276:immunology; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged
D000907:Antibodies, Bacterial; D001055:Apolipoproteins B; D004269:DNA, Bacterial; D015850:Interleukin-6; D002097:C-Reactive Protein