HBD

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Andre Mickel - One of the best experts on this subject based on the ideXlab platform.

  • comparison of il 1β tnf α HBD 2 and HBD 3 expression in the dental pulp of smokers versus nonsmokers
    Journal of Endodontics, 2017
    Co-Authors: Caroline Ghattas Ayoub, Anita Aminoshariae, Mohammed Bakkar, Santosh K. Ghosh, Tracey L. Bonfield, Catherine A. Demko, Thomas A. Montagnese, Andre Mickel
    Abstract:

    INTRODUCTION To date, the endodontic literature lacks research on the effect of smoking on cytokine and defensin expression in the dental pulp. Therefore, the aim of this study was to investigate the expression of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, human beta defensin (HBD)-2 and HBD-3 in the dental pulp of smokers and compare them with nonsmokers. We hypothesized that cytokine and defensin expression would be reduced in smokers as compared with nonsmokers. METHODS Thirty-two smokers and 37 nonsmokers with endodontic pulpal diagnoses of normal, symptomatic irreversible pulpitis and asymptomatic irreversible pulpitis were included in this cross-sectional study. Samples from pulp chambers were collected and stored in phosphate-buffered saline at -80°C. Luminex was used to measure IL-1β and TNF-α levels. The levels of HBD-2 and HBD-3 were measured using enzyme-linked immunosorbent assay. Marker levels were normalized to protein concentrations and data were analyzed using Kruskal-Wallis test, Mann-Whitney U test, and 2-way analysis of variance (α = 0.05). RESULTS Pulpal concentrations of TNF-α and HBD-2 were significantly lower among smokers (P < .01), whereas no significant difference was observed for IL-1β, or HBD-3. Two-way analysis of covariance revealed that smoking status (P < .001), not endodontic diagnosis (pulpal status), significantly affected TNF-α and HBD-2 levels. CONCLUSIONS This study reported that smokers are immunologically deficient in TNF-α and HBD-2, suggesting that dental pulps of smokers possess limited defense mechanisms, affecting their endodontic prognosis and indicating a cause for their reported inferior outcome.

  • Comparison of IL-1β, TNF-α, HBD-2, and HBD-3 Expression in the Dental Pulp of Smokers Versus Nonsmokers.
    Journal of endodontics, 2017
    Co-Authors: Caroline Ghattas Ayoub, Anita Aminoshariae, Mohammed Bakkar, Santosh K. Ghosh, Tracey L. Bonfield, Catherine A. Demko, Thomas A. Montagnese, Andre Mickel
    Abstract:

    INTRODUCTION To date, the endodontic literature lacks research on the effect of smoking on cytokine and defensin expression in the dental pulp. Therefore, the aim of this study was to investigate the expression of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, human beta defensin (HBD)-2 and HBD-3 in the dental pulp of smokers and compare them with nonsmokers. We hypothesized that cytokine and defensin expression would be reduced in smokers as compared with nonsmokers. METHODS Thirty-two smokers and 37 nonsmokers with endodontic pulpal diagnoses of normal, symptomatic irreversible pulpitis and asymptomatic irreversible pulpitis were included in this cross-sectional study. Samples from pulp chambers were collected and stored in phosphate-buffered saline at -80°C. Luminex was used to measure IL-1β and TNF-α levels. The levels of HBD-2 and HBD-3 were measured using enzyme-linked immunosorbent assay. Marker levels were normalized to protein concentrations and data were analyzed using Kruskal-Wallis test, Mann-Whitney U test, and 2-way analysis of variance (α = 0.05). RESULTS Pulpal concentrations of TNF-α and HBD-2 were significantly lower among smokers (P 

Veronica Zagaclavellina - One of the best experts on this subject based on the ideXlab platform.

Ko Okumura - One of the best experts on this subject based on the ideXlab platform.

  • antimicrobial peptides human β defensin HBD 3 and HBD 4 activate mast cells and increase skin vascular permeability
    European Journal of Immunology, 2007
    Co-Authors: Xuejun Chen, François Niyonsaba, Hiroko Ushio, Mutsuko Hara, Hidenori Yokoi, Kenji Matsumoto, Hirohisa Saito, Isao Nagaoka, Shigaku Ikeda, Ko Okumura
    Abstract:

    Antimicrobial peptides human b-defensins (HBD) are mainly produced by epithelia of several organs including skin, and participate in innate immunity by killing invading pathogens. Besides their microbicidal activities, HBD activate several inflammatory and immune cells. Since HBD are generated by tissues where mast cells are present, we hypothesized that these peptides could activate mast cells. In this study, we demonstrated that both HBD-3 and HBD-4 induced mast cell degranulation, prostaglandin D2 production, intracellular Ca 2+ mobilization and chemotaxis. Furthermore, HBD-3- and HBD-4-induced activation of mast cells was suppressed by pertussis toxin and U-73122, inhibitors for G protein and phospholipase C, respectively. We further revealed that HBD-3 and HBD-4 increased vascular permeability in the skin, which was dependent on the presence of mast cells, because HBD-3 and HBD-4 failed to enhance vascular permeability in mast cell-deficient Ws/Ws rats. We also demonstrated that HBD-3 and HBD-4 induced phosphorylation of MAPK p38 and ERK1/2, which were further required for HBD-mediated mast cell activation, as evidenced by the inhibitory effects of p38 and ERK1/2 inhibitors on mast cell degranulation. Together, these findings suggest the key role of HBD in inflammatory responses by recruiting and activating mast cells, and increasing vascular permeability.

  • Antimicrobial peptides human β‐defensin (HBD)‐3 and HBD‐4 activate mast cells and increase skin vascular permeability
    European journal of immunology, 2007
    Co-Authors: Xuejun Chen, François Niyonsaba, Hiroko Ushio, Mutsuko Hara, Hidenori Yokoi, Kenji Matsumoto, Hirohisa Saito, Isao Nagaoka, Shigaku Ikeda, Ko Okumura
    Abstract:

    Antimicrobial peptides human b-defensins (HBD) are mainly produced by epithelia of several organs including skin, and participate in innate immunity by killing invading pathogens. Besides their microbicidal activities, HBD activate several inflammatory and immune cells. Since HBD are generated by tissues where mast cells are present, we hypothesized that these peptides could activate mast cells. In this study, we demonstrated that both HBD-3 and HBD-4 induced mast cell degranulation, prostaglandin D2 production, intracellular Ca 2+ mobilization and chemotaxis. Furthermore, HBD-3- and HBD-4-induced activation of mast cells was suppressed by pertussis toxin and U-73122, inhibitors for G protein and phospholipase C, respectively. We further revealed that HBD-3 and HBD-4 increased vascular permeability in the skin, which was dependent on the presence of mast cells, because HBD-3 and HBD-4 failed to enhance vascular permeability in mast cell-deficient Ws/Ws rats. We also demonstrated that HBD-3 and HBD-4 induced phosphorylation of MAPK p38 and ERK1/2, which were further required for HBD-mediated mast cell activation, as evidenced by the inhibitory effects of p38 and ERK1/2 inhibitors on mast cell degranulation. Together, these findings suggest the key role of HBD in inflammatory responses by recruiting and activating mast cells, and increasing vascular permeability.

Caroline Ghattas Ayoub - One of the best experts on this subject based on the ideXlab platform.

  • comparison of il 1β tnf α HBD 2 and HBD 3 expression in the dental pulp of smokers versus nonsmokers
    Journal of Endodontics, 2017
    Co-Authors: Caroline Ghattas Ayoub, Anita Aminoshariae, Mohammed Bakkar, Santosh K. Ghosh, Tracey L. Bonfield, Catherine A. Demko, Thomas A. Montagnese, Andre Mickel
    Abstract:

    INTRODUCTION To date, the endodontic literature lacks research on the effect of smoking on cytokine and defensin expression in the dental pulp. Therefore, the aim of this study was to investigate the expression of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, human beta defensin (HBD)-2 and HBD-3 in the dental pulp of smokers and compare them with nonsmokers. We hypothesized that cytokine and defensin expression would be reduced in smokers as compared with nonsmokers. METHODS Thirty-two smokers and 37 nonsmokers with endodontic pulpal diagnoses of normal, symptomatic irreversible pulpitis and asymptomatic irreversible pulpitis were included in this cross-sectional study. Samples from pulp chambers were collected and stored in phosphate-buffered saline at -80°C. Luminex was used to measure IL-1β and TNF-α levels. The levels of HBD-2 and HBD-3 were measured using enzyme-linked immunosorbent assay. Marker levels were normalized to protein concentrations and data were analyzed using Kruskal-Wallis test, Mann-Whitney U test, and 2-way analysis of variance (α = 0.05). RESULTS Pulpal concentrations of TNF-α and HBD-2 were significantly lower among smokers (P < .01), whereas no significant difference was observed for IL-1β, or HBD-3. Two-way analysis of covariance revealed that smoking status (P < .001), not endodontic diagnosis (pulpal status), significantly affected TNF-α and HBD-2 levels. CONCLUSIONS This study reported that smokers are immunologically deficient in TNF-α and HBD-2, suggesting that dental pulps of smokers possess limited defense mechanisms, affecting their endodontic prognosis and indicating a cause for their reported inferior outcome.

  • Comparison of IL-1β, TNF-α, HBD-2, and HBD-3 Expression in the Dental Pulp of Smokers Versus Nonsmokers.
    Journal of endodontics, 2017
    Co-Authors: Caroline Ghattas Ayoub, Anita Aminoshariae, Mohammed Bakkar, Santosh K. Ghosh, Tracey L. Bonfield, Catherine A. Demko, Thomas A. Montagnese, Andre Mickel
    Abstract:

    INTRODUCTION To date, the endodontic literature lacks research on the effect of smoking on cytokine and defensin expression in the dental pulp. Therefore, the aim of this study was to investigate the expression of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, human beta defensin (HBD)-2 and HBD-3 in the dental pulp of smokers and compare them with nonsmokers. We hypothesized that cytokine and defensin expression would be reduced in smokers as compared with nonsmokers. METHODS Thirty-two smokers and 37 nonsmokers with endodontic pulpal diagnoses of normal, symptomatic irreversible pulpitis and asymptomatic irreversible pulpitis were included in this cross-sectional study. Samples from pulp chambers were collected and stored in phosphate-buffered saline at -80°C. Luminex was used to measure IL-1β and TNF-α levels. The levels of HBD-2 and HBD-3 were measured using enzyme-linked immunosorbent assay. Marker levels were normalized to protein concentrations and data were analyzed using Kruskal-Wallis test, Mann-Whitney U test, and 2-way analysis of variance (α = 0.05). RESULTS Pulpal concentrations of TNF-α and HBD-2 were significantly lower among smokers (P 

Pilar Floresespinosa - One of the best experts on this subject based on the ideXlab platform.