Cross-reactivity of GroEL antibodies with human heat shock protein 60 and quantification of pathogens in atherosclerosis

被引:93
作者
Ford, PJ [1 ]
Gemmell, E [1 ]
Hamlet, SM [1 ]
Hasan, A [1 ]
Walker, PJ [1 ]
West, MJ [1 ]
Cullinan, MP [1 ]
Seymour, GJ [1 ]
机构
[1] Univ Queensland, Sch Dent, Brisbane, Qld 4072, Australia
来源
ORAL MICROBIOLOGY AND IMMUNOLOGY | 2005年 / 20卷 / 05期
关键词
antibody responses; atherosclerosis; heat shock proteins; molecular mimicry; periodontal immunology;
D O I
10.1111/j.1399-302X.2005.00230.x
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Background/aims: Chronic infections such as those caused by Chlamydia pneumoniae and periodontopathic bacteria such as Porphyromonas gingivalis have been associated with atherosclerosis, possibly due to cross-reactivity of the immune response to bacterial GroEL with human heat shock protein (hHSP) 60. Methods: We examined the cross-reactivity of anti-GroEL and anti-P. gingivalis antibodies with hHSP60 in atherosclerosis patients and quantified a panel of six pathogens in atheromas. Results: After absorption of plasma samples with hHSP60, there were variable reductions in the levels of anti-GroEL and anti-P. gingivalis antibodies, suggesting that these antibodies cross-reacted with hHSP60. All of the artery specimens were positive for P. gingivalis. Fusobacterium nucleatum, Tannerella forsythia, C. pneumoniae, Helicobacter pylori, and Haemophilus influenzae were found in 84%, 48%, 28%, 4%, and 4% of arteries, respectively. The prevalence of the three periodontopathic microorganisms, P. gingivalis, F. nucleatum and T. forsythia, was significantly higher than that of the remaining three microorganisms. Conclusions: These results support the hypothesis that in some patients, cross-reactivity of the immune response to bacterial HSPs including those of periodontal pathogens, with arterial endothelial cells expressing hHSP60 may be a possible mechanism for the association between atherosclerosis and periodontal infection.
引用
收藏
页码:296 / 302
页数:7
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