King's College London

Research portal

Cytokines Elicited by HSP60 in Periodontitis with and without Coronary Heart Disease

Research output: Contribution to journalArticle

Standard

Cytokines Elicited by HSP60 in Periodontitis with and without Coronary Heart Disease. / Hasan, Adam; Sadoh, Danesi; Jones, Bret.

In: Journal of Immune Based Therapies, Vaccines and Antimicrobials, Vol. 3, No. 1, 01.2014.

Research output: Contribution to journalArticle

Harvard

Hasan, A, Sadoh, D & Jones, B 2014, 'Cytokines Elicited by HSP60 in Periodontitis with and without Coronary Heart Disease', Journal of Immune Based Therapies, Vaccines and Antimicrobials, vol. 3, no. 1. https://doi.org/10.4236/jibtva.2014.31001

APA

Hasan, A., Sadoh, D., & Jones, B. (2014). Cytokines Elicited by HSP60 in Periodontitis with and without Coronary Heart Disease. Journal of Immune Based Therapies, Vaccines and Antimicrobials, 3(1). https://doi.org/10.4236/jibtva.2014.31001

Vancouver

Hasan A, Sadoh D, Jones B. Cytokines Elicited by HSP60 in Periodontitis with and without Coronary Heart Disease. Journal of Immune Based Therapies, Vaccines and Antimicrobials. 2014 Jan;3(1). https://doi.org/10.4236/jibtva.2014.31001

Author

Hasan, Adam ; Sadoh, Danesi ; Jones, Bret. / Cytokines Elicited by HSP60 in Periodontitis with and without Coronary Heart Disease. In: Journal of Immune Based Therapies, Vaccines and Antimicrobials. 2014 ; Vol. 3, No. 1.

Bibtex Download

@article{63ab1a2d8a8b4e7aa24c989ae2c479f9,
title = "Cytokines Elicited by HSP60 in Periodontitis with and without Coronary Heart Disease",
abstract = "The human 60 kDa and microbial 65 kDa heat shock proteins (HSP) have been implicated in the pathogenesis of chronic periodontitis (CP) and coronary heart disease (CHD). We have studied 100 subjects: Group (a) consisted of patients with gingivitis (n = 25), group (b) were patients with CP (n = 25), group (c) patients with CHD and gingivitis (n = 25) and group (d) patients with CHD and CP (n = 25). PBMCs separated from peripheral blood were stimulated with medium, PMA/ionomycin, human HSP60, microbial HSP65, or no stimulus for 18 hours before intracellular IL-2, IFN-γ, TNF-α, IL-4, IL-5, or IL-17 were detected by flow cytometry. The mean fluorescence intensity (MFLI) for intracellular TNF-α was significantly increased when PBMC were stimulated with human HSP60 amongst the four groups (p = 0.001, ANOVA); pairwise comparisons revealed significant differences in MFLI between the gingivitis group and the CP (p = 0.017); between gingivitis and ging/CHD (p = 0.001) as well; but no significant difference between the CP and CP/CHD (p = 0.442). There was no significant difference in intracellular expression of IL-17, or any of the other cytokines tested; and the MFLI for HSP-stimulated were comparable to unstimulated cultures. When heat-labile human HSP60 was heated, intracellular cellular TNF-α expression was abrogated. In contrast, heat-stable LPS elicited TNF-α expression from monocytes in bulk cultures in all groups. These results suggest that the cytokine expression was dependent on human HSP60 and not LPS. Serum CRP was significantly associated with MFLI of intracellular TNF-α in CP patients (rs = 0.665, p = 0.026) and CP/CHD (rs = 0.699, p = 0.011). We conclude that human HSP60 elicits increased monocytic expression of TNF-α in patients with CP, CP/CHD or ging/CHD compared to patients with gingivitis. Since the marker of inflammation, namely CRP correlates with CP with or without CHD and not with mild chronic gingivitis or ging/CHD, this suggests that human HSP60-induced production of TNF-α is associated with CP and not CHD. There was no significant difference in intracellular expression of IL-17.",
keywords = "HSP60, Periodontitis, Coronary Artery Disease, CYTOKINES",
author = "Adam Hasan and Danesi Sadoh and Bret Jones",
year = "2014",
month = jan,
doi = "10.4236/jibtva.2014.31001",
language = "English",
volume = "3",
journal = "Journal of Immune Based Therapies, Vaccines and Antimicrobials",
number = "1",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - Cytokines Elicited by HSP60 in Periodontitis with and without Coronary Heart Disease

AU - Hasan, Adam

AU - Sadoh, Danesi

AU - Jones, Bret

PY - 2014/1

Y1 - 2014/1

N2 - The human 60 kDa and microbial 65 kDa heat shock proteins (HSP) have been implicated in the pathogenesis of chronic periodontitis (CP) and coronary heart disease (CHD). We have studied 100 subjects: Group (a) consisted of patients with gingivitis (n = 25), group (b) were patients with CP (n = 25), group (c) patients with CHD and gingivitis (n = 25) and group (d) patients with CHD and CP (n = 25). PBMCs separated from peripheral blood were stimulated with medium, PMA/ionomycin, human HSP60, microbial HSP65, or no stimulus for 18 hours before intracellular IL-2, IFN-γ, TNF-α, IL-4, IL-5, or IL-17 were detected by flow cytometry. The mean fluorescence intensity (MFLI) for intracellular TNF-α was significantly increased when PBMC were stimulated with human HSP60 amongst the four groups (p = 0.001, ANOVA); pairwise comparisons revealed significant differences in MFLI between the gingivitis group and the CP (p = 0.017); between gingivitis and ging/CHD (p = 0.001) as well; but no significant difference between the CP and CP/CHD (p = 0.442). There was no significant difference in intracellular expression of IL-17, or any of the other cytokines tested; and the MFLI for HSP-stimulated were comparable to unstimulated cultures. When heat-labile human HSP60 was heated, intracellular cellular TNF-α expression was abrogated. In contrast, heat-stable LPS elicited TNF-α expression from monocytes in bulk cultures in all groups. These results suggest that the cytokine expression was dependent on human HSP60 and not LPS. Serum CRP was significantly associated with MFLI of intracellular TNF-α in CP patients (rs = 0.665, p = 0.026) and CP/CHD (rs = 0.699, p = 0.011). We conclude that human HSP60 elicits increased monocytic expression of TNF-α in patients with CP, CP/CHD or ging/CHD compared to patients with gingivitis. Since the marker of inflammation, namely CRP correlates with CP with or without CHD and not with mild chronic gingivitis or ging/CHD, this suggests that human HSP60-induced production of TNF-α is associated with CP and not CHD. There was no significant difference in intracellular expression of IL-17.

AB - The human 60 kDa and microbial 65 kDa heat shock proteins (HSP) have been implicated in the pathogenesis of chronic periodontitis (CP) and coronary heart disease (CHD). We have studied 100 subjects: Group (a) consisted of patients with gingivitis (n = 25), group (b) were patients with CP (n = 25), group (c) patients with CHD and gingivitis (n = 25) and group (d) patients with CHD and CP (n = 25). PBMCs separated from peripheral blood were stimulated with medium, PMA/ionomycin, human HSP60, microbial HSP65, or no stimulus for 18 hours before intracellular IL-2, IFN-γ, TNF-α, IL-4, IL-5, or IL-17 were detected by flow cytometry. The mean fluorescence intensity (MFLI) for intracellular TNF-α was significantly increased when PBMC were stimulated with human HSP60 amongst the four groups (p = 0.001, ANOVA); pairwise comparisons revealed significant differences in MFLI between the gingivitis group and the CP (p = 0.017); between gingivitis and ging/CHD (p = 0.001) as well; but no significant difference between the CP and CP/CHD (p = 0.442). There was no significant difference in intracellular expression of IL-17, or any of the other cytokines tested; and the MFLI for HSP-stimulated were comparable to unstimulated cultures. When heat-labile human HSP60 was heated, intracellular cellular TNF-α expression was abrogated. In contrast, heat-stable LPS elicited TNF-α expression from monocytes in bulk cultures in all groups. These results suggest that the cytokine expression was dependent on human HSP60 and not LPS. Serum CRP was significantly associated with MFLI of intracellular TNF-α in CP patients (rs = 0.665, p = 0.026) and CP/CHD (rs = 0.699, p = 0.011). We conclude that human HSP60 elicits increased monocytic expression of TNF-α in patients with CP, CP/CHD or ging/CHD compared to patients with gingivitis. Since the marker of inflammation, namely CRP correlates with CP with or without CHD and not with mild chronic gingivitis or ging/CHD, this suggests that human HSP60-induced production of TNF-α is associated with CP and not CHD. There was no significant difference in intracellular expression of IL-17.

KW - HSP60

KW - Periodontitis

KW - Coronary Artery Disease

KW - CYTOKINES

U2 - 10.4236/jibtva.2014.31001

DO - 10.4236/jibtva.2014.31001

M3 - Article

VL - 3

JO - Journal of Immune Based Therapies, Vaccines and Antimicrobials

JF - Journal of Immune Based Therapies, Vaccines and Antimicrobials

IS - 1

ER -

View graph of relations

© 2018 King's College London | Strand | London WC2R 2LS | England | United Kingdom | Tel +44 (0)20 7836 5454