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.

Lenzi, C., Palazzuoli, A., Giordano, N.G., Alegente, G., Gonnelli, C., Campagna, M.S., et al. (2006). H pylori infection and systemic antibodies to CagA and heat shock protein 60 in patients with coronary heart disease. WORLD JOURNAL OF GASTROENTEROLOGY, 12(48), 7815-7820 [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

LENZI, CRISTINA;PALAZZUOLI, ALBERTO;GIORDANO, NICOLA GIUSEPPE;GONNELLI, CATIA;CAMPAGNA, MARIA STELLA;SANTUCCI, ANNALISA;PAPAKOSTAS, PANAGIOTIS;ROLLO, FABIO;NUTI, RANUCCIO;FIGURA, NATALE
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.
Lenzi, C., Palazzuoli, A., Giordano, N.G., Alegente, G., Gonnelli, C., Campagna, M.S., et al. (2006). H pylori infection and systemic antibodies to CagA and heat shock protein 60 in patients with coronary heart disease. WORLD JOURNAL OF GASTROENTEROLOGY, 12(48), 7815-7820 [10.3748/wjg.v12.i48.7815].
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11365/21664
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