Association of Helicobacter pylori infection with systemic inflammation and endothelial dysfunction in healthy male subjects.
OBJECTIVE
The goal of the present study was to determine whether seropositivity to Helicobacter pylori (HP), Chlamydia pneumoniae (CP), and cytomegalovirus (CMV) is associated with systemic inflammation and endothelial dysfunction in healthy male subjects.


BACKGROUND
Chronic infection with certain bacteria and viruses may play an important role in inflammation as the pathogenesis of atherosclerosis.


METHODS
The serum levels of immunoglobulin G antibodies to HP, CP, CMV, high-sensitivity C-reactive protein, soluble intercellular adhesion molecule-1, and soluble vascular cell adhesion molecule-1 were determined in 81 healthy Japanese men (40 +/- 10 years of age). High-frequency ultrasonographic imaging of the brachial artery was used to study endothelium-dependent (flow-mediated vasodilation) and endothelium-independent (nitroglycerin-induced) vasodilation.


RESULTS
Prevalences of seropositive antibodies to HP, CP, and CMV were 67.9%, 61.7%, and 56.8%, respectively. Infection with HP, CP, or CMV had no relationship with age, blood pressure, or level of serum glucose, lipid, or soluble vascular cell adhesion molecule-1. The levels of C-reactive protein and soluble intercellular adhesion molecule-1 were significantly higher, and flow-mediated vasodilation was significantly lower in subjects with seropositive antibodies to HP than in subjects with seronegative antibodies to HP. Endothelium-independent vasodilation was similar in both groups.


CONCLUSIONS
Chronic infection with HP may be involved in the development of the atherosclerosis via endothelial dysfunction and systemic and vascular inflammation.
Oshima
Tetsuya
T
Department of Clinical Laboratory Medicine, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan. teto@hiroshima-u.ac.jp
Ozono
Ryoji
R
Yano
Yoko
Y
Oishi
Yoshihiko
Y
Teragawa
Hiroki
H
Higashi
Yukihito
Y
Yoshizumi
Masao
M
Kambe
Masayuki
M
D000328:Adult; D000907:Antibodies, Bacterial / Q000097:blood; D000914:Antibodies, Viral / Q000097:blood; D001161:Arteriosclerosis / Q000209:etiology; D002097:C-Reactive Protein / Q000032:analysis; D016993:Chlamydophila pneumoniae / Q000276:immunology; D003587:Cytomegalovirus / Q000276:immunology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D016481:Helicobacter Infections / Q000097:blood / Q000150:complications* / Q000276:immunology / Q000503:physiopathology; D016480:Helicobacter pylori / Q000276:immunology; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D007249:Inflammation / Q000209:etiology*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008297:Male; D016036:Seroepidemiologic Studies; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D014664:Vasodilation / Q000502:physiology
D000907:Antibodies, Bacterial; D000914:Antibodies, Viral; D007074:Immunoglobulin G; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein