title: H pylori infection and systemic antibodies to CagA and heat shock protein 60 in patients with coronary heart disease.
abstract: OBJECTIVE
  to determine the overall prevalence of H pylori and CagA positive H pylori infection and the prevalence of other bacterial and viral causes of chronic infection in patients with coronary heart disease (CHD), and the potential role of anti-heat-shock protein 60 (Hsp60) antibody response to these proteins in increasing the risk of CHD development.
  
  
  METHODS
  Eighty patients with CHD and 160 controls were employed. We also compared the levels of anti-heat-shock protein 60 (Hsp60) antibodies in the two groups. The H pylori infection and the CagA status were determined serologically, using commercially available enzyme-linked immunosorbent assays (ELISA), and a Western blotting method developed in our laboratory. Systemic antibodies to Hsp60 were determined by a sandwich ELISA, using a polyclonal antibody to Hsp60 to sensitise polystyrene plates and a commercially available human Hsp60 as an antigen.
  
  
  RESULTS
  The overall prevalence of H pylori infection was 78.7% (n = 63) in patients and 76.2% (n = 122) in controls (P = 0.07). Patients infected by CagA-positive (CagA+) H pylori strains were 71.4% (n = 45) vs 52.4% of infected controls (P = 0.030, OR = 2.27). Systemic levels of IgG to Hsp60 were increased in H pylori-negative patients compared with uninfected controls (P < 0.001) and CagA-positive infected patients compared with CagA-positive infected controls (P = 0.007).
  
  
  CONCLUSIONS
  CagA positive H pylori infection may concur to the development of CHD; high levels of anti-Hsp60 antibodies may constitute a marker and/or a concomitant pathogenic factor of the disease.
authors.affiliation: Department of Internal Medicine Endocrine-Metabolic Sciences and Biochemistry, University of Siena, Siena, Italy.
authors.forename: Cristina
authors.initials: C
authors.lastname: Lenzi
authors.forename: Alberto
authors.initials: A
authors.lastname: Palazzuoli
authors.forename: Nicola
authors.initials: N
authors.lastname: Giordano
authors.forename: Giuliano
authors.initials: G
authors.lastname: Alegente
authors.forename: Catia
authors.initials: C
authors.lastname: Gonnelli
authors.forename: Maria-Stella
authors.initials: MS
authors.lastname: Campagna
authors.forename: Annalisa
authors.initials: A
authors.lastname: Santucci
authors.forename: Michele
authors.initials: M
authors.lastname: Sozzi
authors.forename: Panagiotis
authors.initials: P
authors.lastname: Papakostas
authors.forename: Fabio
authors.initials: F
authors.lastname: Rollo
authors.forename: Ranuccio
authors.initials: R
authors.lastname: Nuti
authors.forename: Natale
authors.initials: N
authors.lastname: Figura
mesh_terms: D000328:Adult; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood*; D000942:Antigens, Bacterial / Q000276:immunology* / Q000502:physiology; D001426:Bacterial Proteins / Q000276:immunology* / Q000502:physiology; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D018834:Chaperonin 60 / Q000276:immunology* / Q000502:physiology; D016993:Chlamydophila pneumoniae / Q000472:pathogenicity; D003327:Coronary Disease / Q000097:blood / Q000209:etiology* / Q000276:immunology*; D003587:Cytomegalovirus / Q000472:pathogenicity; D005260:Female; D016481:Helicobacter Infections / Q000150:complications* / Q000276:immunology; D016480:Helicobacter pylori / Q000276:immunology* / Q000472:pathogenicity; D004854:Herpesvirus 4, Human / Q000472:pathogenicity; D006801:Humans; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D012307:Risk Factors; D018139:Simplexvirus / Q000472:pathogenicity
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D015415:Biomarkers; D018834:Chaperonin 60; C080866:cagA protein, Helicobacter pylori