Epitope Mapping of <i>Porphyromonas gingivalis</i> Heat-shock Protein and Human Heat-shock Protein in Human Atherosclerosis

Choi, Jeomil; Chung, Sungwook; Kang, Hyen Sam; Rhim, Byung Yong; Park, Y.-M.; Kim, U.-S.; Kim, S.-J.

doi:10.1177/154405910408301209

Cited by 46 publications

(47 citation statements)

References 19 publications

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“…Based on our series observations (14,15,17,19), we hypothesized that the Pep19 may be a dominant epitope from which the epitope-specific immune response to subdominant epitopes may diversify sequentially into autoimmune responses directed at human neoepitopes in P. gingivalis-induced periodontitis and autoimmune diseases. To clarify this phenomenon and to identify the mechanism to support the hypothesis, a study has been devised for two independent investigations; a cross-sectional analysis on clinical subjects and a prospective analysis on experimental periodontitis, each being subdivided further into two additional independent observations.…”

Section: Discussionmentioning

confidence: 99%

Pep19 drives epitope spreading in periodontitis and periodontitis‐associated autoimmune diseases

G.S.Cha

Jeong

et al. 2015

J of Periodontal Research

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Taken together, epitope spreading to Hu19, Hu9 and ox-LDL provoked by Pep19 could be proposed as a solid phenomenon observed in P. gingivalis-induced chronic periodontitis and infection-induced autoimmune diseases in a reproducible and predictable manner. T-cell proliferative activity to these peptides and cross-reactivity of anti-Pep19 antibodies to multiple human autoantigens could be proposed as cellular and molecular mechanisms responsible for this phenomenon.

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Section: Discussionmentioning

confidence: 99%

Pep19 drives epitope spreading in periodontitis and periodontitis‐associated autoimmune diseases

G.S.Cha

Jeong

et al. 2015

J of Periodontal Research

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“…Porphyromonas gingivalis HSP60 contains both B-and T-cell epitopes cross-reactive with hHSP60 (Choi et al 2004). Furthermore, T-cell lines derived from atherosclerotic plaques are cross-reactive between human HSP and GroEL (Ford et al 2005).…”

Section: Heat-shock Proteinsmentioning

confidence: 99%

Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases

Schenkein

Loos

2013

Journal of Periodontology

159

118

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Inflammatory mechanisms linking periodontal diseases to cardiovascular diseasesSchenkein HA, Loos BG. Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases. AbstractAims: In this article, inflammatory mechanisms that link periodontal diseases to cardiovascular diseases are reviewed. Methods: This article is a literature review. Results: Studies in the literature implicate a number of possible mechanisms that could be responsible for increased inflammatory responses in atheromatous lesions due to periodontal infections. These include increased systemic levels of inflammatory mediators stimulated by bacteria and their products at sites distant from the oral cavity, elevated thrombotic and hemostatic markers that promote a prothrombotic state and inflammation, cross-reactive systemic antibodies that promote inflammation and interact with the atheroma, promotion of dyslipidemia with consequent increases in pro-inflammatory lipid classes and subclasses, and common genetic susceptibility factors present in both disease leading to increased inflammatory responses. Conclusions: Such mechanisms may be thought to act in concert to increase systemic inflammation in periodontal disease and to promote or exacerbate atherogenesis. However, proof that the increase in systemic inflammation attributable to periodontitis impacts inflammatory responses during atheroma development, thrombotic events or myocardial infarction or stroke is lacking.

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“…N.D., not detectable. subjects (25). HSP60 is conserved across species, and immune reactions to HSP60 have been widely described in infectious disease due to bacteria that express HSP60 (26).…”

Section: Discussionmentioning

confidence: 99%

Serum Antibodies against Porphyromonas gingivalis GroEL are Insufficient to Induce P.gingivalis-accelerated Atherosclerosis

et al. 2013

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Periodontitis is associated with an increased risk of atherosclerosis, and accumulating evidence suggests a positive association between anti-heat shock protein 60 autoantibodies and atherosclerosis in humans. Heat shock proteins of the GroEL or HSP60 class are highly conserved proteins essential to all living organisms. In this study, we examined the effects of immunization with recombinant HSP60 from Porphyromonas gingivalis on antibody responses and the development of atherosclerosis.Atherosclerosis was examined in BALB/c mice fed a high-fat diet or a regular chow diet following subcutaneous immunization with GroEL or intravenous injection with P. gingivalis. The proximal aorta lesion area, serum levels of anti-GroEL antibodies, CRP and MCP-1 levels, expression of HSPs, and inflammatory mediator expression in aorta were measured.Early atherosclerotic lesion area was substantially lower in HFD-fed mice immunized with GroEL compared to P. gingivalis-challenged mice, although significant atherosclerotic lesions, serum immunoglobulin G responses to GroEL, and HSP60 were detected in GroEL-immunized mice. Immunohistochemical staining confirmed strong HSP60 expression in the vascular wall of HFD-fed mice compared to RD-fed mice. Although immunization of the HFD-fed mice with GroEL slightly enhanced serum MCP-1 secretion as well as CD40/40L and LOX-1 expression in the aorta, it did not affect serum CRP levels.These results suggest that immune response cross-reactivity to bacterial HSPs, including periodontal pathogens, with arterial endothelial cells expressing HSP60 are not associated with atherosclerosis severity caused by P. gingivalis challenge. This may explain why antibody responses to bacterial HSPs are an unlikely major risk factor for coronary artery disease.

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Epitope Mapping of Porphyromonas gingivalis Heat-shock Protein and Human Heat-shock Protein in Human Atherosclerosis

Cited by 46 publications

References 19 publications

Pep19 drives epitope spreading in periodontitis and periodontitis‐associated autoimmune diseases

Pep19 drives epitope spreading in periodontitis and periodontitis‐associated autoimmune diseases

Inflammatory mechanisms linking periodontal diseases to cardiovascular diseases

Serum Antibodies against Porphyromonas gingivalis GroEL are Insufficient to Induce P.gingivalis-accelerated Atherosclerosis

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