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. 2006 Dec 28;12(48):7815-20.
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

Affiliations

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

Cristina Lenzi et al. World J Gastroenterol. .

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.

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Figures

Figure 1
Figure 1
Prevalence of overall H pylori and CagA+ H pylori infection in patients and controls.
Figure 2
Figure 2
Mean levels (in optical density) of anti-Hsp60 systemic antibodies in patients and controls.

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References

    1. Pasceri V, Cammarota G, Patti G, Cuoco L, Gasbarrini A, Grillo RL, Fedeli G, Gasbarrini G, Maseri A. Association of virulent Helicobacter pylori strains with ischemic heart disease. Circulation. 1998;97:1675–1679. - PubMed
    1. Gunn M, Stephens JC, Thompson JR, Rathbone BJ, Samani NJ. Significant association of cagA positive Helicobacter pylori strains with risk of premature myocardial infarction. Heart. 2000;84:267–271. - PMC - PubMed
    1. Epstein SE, Zhou YF, Zhu J. Infection and atherosclerosis: emerging mechanistic paradigms. Circulation. 1999;100:e20–e28. - PubMed
    1. Epstein SE. The multiple mechanisms by which infection may contribute to atherosclerosis development and course. Circ Res. 2002;90:2–4. - PubMed
    1. Graham DY. Campylobacter pylori and peptic ulcer disease. Gastroenterology. 1989;96:615–625. - PubMed

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