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World J Gastroenterol. Dec 28, 2006; 12(48): 7815-7820
Published online Dec 28, 2006. doi: 10.3748/wjg.v12.i48.7815
H pylori infection and systemic antibodies to CagA and heat shock protein 60 in patients with coronary heart disease
Cristina Lenzi, Alberto Palazzuoli, Nicola Giordano, Giuliano Alegente, Catia Gonnelli, Maria Stella Campagna, Annalisa Santucci, Michele Sozzi, Panagiotis Papakostas, Fabio Rollo, Ranuccio Nuti, Natale Figura
Cristina Lenzi, Alberto Palazzuoli, Nicola Giordano, Catia Gonnelli, Maria Stella Campagna, Panagiotis Papakostas, Fabio Rollo, Ranuccio Nuti, Natale Figura, Department of Internal Medicine Endocrine-Metabolic Sciences and Biochemistry, University of Siena, Siena, Italy
Giuliano Alegente, Unit of Microbiology, General Hospital, Siena, Italy
Annalisa Santucci, Department of Molecular Biology, University of Siena, Siena, Italy
Michele Sozzi, Unit of Gastroenterology and Digestive Endoscopy, General Hospital, Trieste, Italy
Supported by a grant from the University of Siena, PAR 2004 “H pylori infection, hosts’ aplotypes of inflammatory cytokines and the risk of ischemic heart disease”
Correspondence to: Natale Figura, Department of Internal Medicine Endocrine-Metabolic Sciences and Biochemistry, University of Siena, Siena, Policlinico S Maria alle Scotte, v.le Bracci, I-53100 Siena, Italy. figura@unisi.it
Telephone: +39-577-585365 Fax: +39-577-233446
Received: October 5, 2006
Revised: October 28, 2006
Accepted: November 30, 2006
Published online: December 28, 2006
Abstract

AIM: 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).

CONCLUSION: 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.

Keywords: H pylori; Coronary heart disease; CagA protein; Heat shock protein 60; Antibody response