title: Association of Helicobacter pylori infection with systemic inflammation and endothelial dysfunction in healthy male subjects.
abstract: 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.
authors.affiliation: Department of Clinical Laboratory Medicine, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan. teto@hiroshima-u.ac.jp
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Oshima
authors.forename: Ryoji
authors.initials: R
authors.lastname: Ozono
authors.forename: Yoko
authors.initials: Y
authors.lastname: Yano
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Oishi
authors.forename: Hiroki
authors.initials: H
authors.lastname: Teragawa
authors.forename: Yukihito
authors.initials: Y
authors.lastname: Higashi
authors.forename: Masao
authors.initials: M
authors.lastname: Yoshizumi
authors.forename: Masayuki
authors.initials: M
authors.lastname: Kambe
mesh_terms: 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
chemical_list: D000907:Antibodies, Bacterial; D000914:Antibodies, Viral; D007074:Immunoglobulin G; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein