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H pylori infection and systemic antibodies to CagA and heat shock protein 60 in patients with coronary heart disease

查看全文 作　　者：Cristina [1]Lenzi;Alberto [1]Palazzuoli;Nicola [1]Giordano;Giuliano [2]Alegente;Catia [1]Gonnelli;Maria Stella [1]Campagna;Annalisa [3]Santucci;Michele [4]Sozzi;Panagiotis [1]Papakostas;Fabio [1]Rollo;Ranuccio [1]Nuti;Natale [1]Figura 高影响力作者 机构地区：[1]Department of In-ternal Medicine Endocrine-Metabolic Sciences and Biochemistry, University of Siena, Siena, Italy;[2]Unit of Microbiology, General Hospital, Siena, Italy;[3]Department of Molecular Biology, University of Siena, Siena, Italy;[4]Unit of Gastroenterology and Digestive Endos-copy, General Hospital, Trieste, Italy高影响力机构 出　　处：《World Journal of Gastroenterology》索引2006年第12卷第48期,共6页高影响力期刊 基　　金：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' 摘　　要：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) anti- body 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 infec- tion 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). Sys-temic 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 con- comitant pathogenic factor of the disease. 关 键 词：幽门螺杆菌 热休克蛋白 冠心病 治疗
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