Title of article
Investigation of Chlamydia pneumoniae DNA, chlamydial lipopolisaccharide antigens, and Helicobacter pylori DNA in atherosclerotic plaques of patients with aortoiliac occlusive disease
Author/Authors
Islam Kaklikkaya، نويسنده , , Islam and Kaklikkaya، نويسنده , , Nese and Buruk، نويسنده , , Kurtulu? and Pulathan، نويسنده , , Zerrin and Koramaz، نويسنده , , Ismail Orhan Aydin، نويسنده , , Faruk and Tosun، نويسنده , , Ilknur and Osman Kilic، نويسنده , , Ali Vefa Ozcan، نويسنده , , Fahri، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2006
Pages
5
From page
105
To page
109
Abstract
Background and Introduction
been suggested that chronic infections may have a role in both the initiation and progression of atherosclerosis. While the majority of available data are focused on coronary artery disease, our aim was to investigate the presence of Chlamydia pneumoniae and Helicobacter pylori in samples from aortoiliac occlusive disease.
s
iliac atherectomy specimens were collected under sterile conditions from 21 patients (19 male, 2 female) undergoing surgery for aortoiliac occlusive disease. Seventeen macroscopically healthy vessels (12 internal mammary arteries, 3 radial arteries, prepared for coronary artery bypass graft, and 2 traumatic artery specimens, one of which was a superficial femoral artery and the other was a radial artery) were used as control. Blood samples for serological assays were obtained immediately before surgery. The polymerase chain reaction (PCR) was employed to search for H. pylori and C. pneumoniae DNA in atherosclerotic plaques and healthy vessel samples. Group-specific chlamydial lipopolysaccharide (LPS) antigens in atherosclerotic plaques and in healthy vessel samples and serum IgG antibodies to chlamydial LPS were determined by using a commercially available enzyme-linked immunosorbent assay (ELISA). Antibodies to H. pylori were also tested in all cases by means of an in-house ELISA.
s
dial LPS and DNA were detected in 6 of 21 (28.57%) atherosclerotic lesions using ELISA or PCR, respectively. There was no evidence of H. pylori DNA in any plaque specimens. All cases in which C. pneumoniae DNA was positive were also seropositive for antichlamydial LPS. Neither C. pneumoniae DNA nor antigen nor H. pylori DNA was found in the macroscopically healthy samples.
sion
sults suggest that C. pneumoniae but not, as proposed, H. pylori may be involved in the pathogenesis of aortoiliac atherosclerosis.
Keywords
Aortoiliac occlusive disease , Helicobacter pylori , Chlamydia Pneumoniae , atherosclerosis
Journal title
Cardiovascular Pathology
Serial Year
2006
Journal title
Cardiovascular Pathology
Record number
1844943
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