Immune responses to heat shock protein in <i>Porphyromonas gingivalis</i>‐infected periodontitis and atherosclerosis patients

Chung, Sungwook; Kang, Hyen Sam; Park, Hae Ryoun; Kim, Sung-Jo; Kim, Soojin; Choi, Jeomil

doi:10.1034/j.1600-0765.2003.00664.x

Cited by 36 publications

(37 citation statements)

References 23 publications

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“…Many population-based studies showed a strong correlation between ATS and high levels of soluble, circulating HSP60 [62][63][64][65][66] as well as of anti-HSP60 antibodies [65][66][67][68][69]. Both chaperonin and anti-chaperonin antibodies have been shown to elicit production of pro-inflammatory cytokines [59,70,71]. An indirect confirmation of the pro-atherogenic role of HSP60 and anti-HSP60 antibodies came from studies done with mice immunized against human HSP60.…”

Section: Hsp60 and Its Bacterial Counterpart Are Pro-atherogenic Molementioning

confidence: 95%

“…The probable sources of these autoantibodies can be infections by distinct pathogens in various locations, such as lung (Chlamydia pneumonia [67,75] or Mycobacterium tuberculosis [75][76][77]), genital tract (Chlamydia trachomatis [78,79]), oral cavity (Porphyromonas gingivalis [70,80]), and stomach (Helicobacter pylori [81,82]). Also, antibodies that can destroy endothelial cells overexpressing HSP60 have been observed in viral (e.g.…”

Section: Hsp60 and Its Bacterial Counterpart Are Pro-atherogenic Molementioning

confidence: 99%

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Heat Shock Protein-60 and Risk for Cardiovascular Disease

Rizzo¹,

Macario²,

Macario³

et al. 2011

CPD

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Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. There is growing evidence that molecular chaperones, many of which are heat shock proteins HSPs, are involved in CVD pathogenesis. In this review we focus on HSP60, the human mitochondrial chaperone that also displays extramitochondrial and extracellular functions. HSP60 is typically cytoprotective but a number of stress conditions determine its conversion to a potentially toxic molecule for cells and tissues. We present illustrative examples of specific subtypes of CVD where HSP60 is implicated in the initiation and/or progression of disease. The data not only indicate a pathogenic role for HSP60 but also its potential as a biomarker with applications for diagnosis, assessing prognosis and response to treatment, as well as for preventing and treating CVD.

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Section: Hsp60 and Its Bacterial Counterpart Are Pro-atherogenic Molementioning

confidence: 95%

Section: Hsp60 and Its Bacterial Counterpart Are Pro-atherogenic Molementioning

confidence: 99%

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Rizzo¹,

Macario²,

Macario³

et al. 2011

CPD

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show abstract

“…[7,8,31,32]. Yet, the involvement of Hp-infection or Hp-HSP60 in atherosclerosis is still controversial [23,33e35].…”

Section: Discussionmentioning

confidence: 99%

Antibodies against heat shock protein 60 derived from Helicobacter pylori: Diagnostic implications in cardiovascular disease

Okada

Ayada

Usui

et al. 2007

Journal of Autoimmunity

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Immune responses against heat shock protein 60 (HSP60) of pathogen-origin are thought to be defensive events which, due to molecular mimicry, misdirect to a human counterpart. Therefore, atherosclerosis may be serologically predicted by anti-HSP60 antibodies (Abs). In the present study, we analyzed the clinical prevalence of the serum IgG Abs against Helicobacter pylori (Hp)-derived HSP60 (Hp-HSP60) or its peptide fragments in patients with cardiovascular disease (CVD; n=250), as compared to those in age- and gender-matched non-CVD patients (n=293). Anti-Hp cell lysate Abs frequently appeared in Hp-infected patients who were not associated with CVD. In contrast, Abs against the particular amino acid sequence Hp-HSP60(II3) (II3 region, Glu(141)-Leu(160), in Hp-HSP60) predominantly appeared in CVD patients, as well as IgG anti-human HSP60 (Hu-HSP60(w)). Furthermore, neither titer of anti-Hp-HSP60(II3) nor anti-Hu-HSP60(w) Abs was correlated with the levels of high sensitivity C-reactive protein (hsCRP). This data strongly suggested that IgG anti-Hp-HSP60(II3) Abs cross-reacted with Hu-HSP60(w) were independent diagnostic markers relevant to CVD. Further, the 20 amino acid residues (Glu(141)-Leu(160)) might be predominant CVD-associated epitopes that induce anti-Hu-HSP60 auto-Abs, whose location was predicted in the tertiary structure of Hu-HSP60.

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“…3,20,21) Hypothesized mechanisms include the direct effect of a subgingival biofilm or an indirect effect through an immunologic response and activation of inflammation is involved in the pathogenesis of atherosclerotic plaque formation. 20,21) Endothelial dysfunction is the first step in the development of atherosclerosis. Periodontitis has been demonstrated to be related with endothelial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Prediagnostic Plasma Antibody Levels to Periodontopathic Bacteria and Risk of Coronary Heart Disease

et al. 2012

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SummaryMany epidemiological studies have indicated that periodontitis is an important risk factor for coronary heart disease (CHD). We examined whether plasma antibody levels to 3 major periodontal pathogens, Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia predicted the risk of CHD events.A nested case-control research design (case: n = 191, control: n = 382), by matching gender, age, study area, date of blood collection, and time since last meal at blood collection, was employed in a large cohort of Japanese community residents.Antibody levels of periodontopathic bacteria were associated with risk of CHD after adjusting for BMI, smoking status, alcohol intake, history of hypertension, history of diabetes mellitus, exercise during leisure time, and perceived mental stress. The association was different by age subgroup. For subjects aged 40-55 years, the medium (31.7-184.9 U/ mL) or high tertile plasma antibody level (> 184.9 U/mL) of A. actinomycetemcomitans showed higher risk of CHD (medium: OR = 3.72; 95% CI = 1.20-11.56, high: OR = 4.64; 95% CI = 1.52-14.18) than the low tertile level (< 31.7 U/ mL). The ORs of CHD incidence became higher with an increase in IgG level of A. actinomycetemcomitans (P for trend = 0.007). For subjects aged 56-69 years, the high tertile level (> 414.1 U/mL) of P. intermedia was associated with higher risk of CHD (OR = 2.65; 95% CI = 1.18-5.94) in a dose-response fashion (P for trend = 0.007).The possible role of periodontopathic bacteria as a risk factor for CHD incidence was suggested by the results of this study by the elevated antibody level to these bacteria with the increased risk of CHD. (Int Heart J 2012; 53: 209-214)

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Immune responses to heat shock protein in Porphyromonas gingivalis‐infected periodontitis and atherosclerosis patients

Abstract: These observations suggest the modulating effect of P. gingivalis hsp60 in the immunopathogenesis of periodontitis and atherosclerosis.

Cited by 36 publications

References 23 publications

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Heat Shock Protein-60 and Risk for Cardiovascular Disease

Antibodies against heat shock protein 60 derived from Helicobacter pylori: Diagnostic implications in cardiovascular disease

Prediagnostic Plasma Antibody Levels to Periodontopathic Bacteria and Risk of Coronary Heart Disease

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