Cholesterol crystals enhance TLR2-and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis

Research output: Contribution to journal › Journal article › Research › peer-review

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Cholesterol crystals enhance TLR2-and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis. / Køllgaard, Tania Maria Simonsen; Enevold, Christian; Bendtzen, Klaus; Hansen, Peter R.; Givskov, Michael; Holmstrup, Palle; Nielsen, Claus H.

In: P L o S One, Vol. 12, No. 2, 0172773, 24.02.2017.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Køllgaard, TMS, Enevold, C, Bendtzen, K, Hansen, PR, Givskov, M, Holmstrup, P & Nielsen, CH 2017, 'Cholesterol crystals enhance TLR2-and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis', P L o S One, vol. 12, no. 2, 0172773. https://doi.org/10.1371/journal.pone.0172773

APA

Køllgaard, T. M. S., Enevold, C., Bendtzen, K., Hansen, P. R., Givskov, M., Holmstrup, P., & Nielsen, C. H. (2017). Cholesterol crystals enhance TLR2-and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis. P L o S One, 12(2), [0172773]. https://doi.org/10.1371/journal.pone.0172773

Vancouver

Køllgaard TMS, Enevold C, Bendtzen K, Hansen PR, Givskov M, Holmstrup P et al. Cholesterol crystals enhance TLR2-and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis. P L o S One. 2017 Feb 24;12(2). 0172773. https://doi.org/10.1371/journal.pone.0172773

Author

Køllgaard, Tania Maria Simonsen ; Enevold, Christian ; Bendtzen, Klaus ; Hansen, Peter R. ; Givskov, Michael ; Holmstrup, Palle ; Nielsen, Claus H. / Cholesterol crystals enhance TLR2-and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis. In: P L o S One. 2017 ; Vol. 12, No. 2.

Bibtex

@article{0dabb8c91e7d46fea8194e94b54b141d,
title = "Cholesterol crystals enhance TLR2-and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis",
abstract = "Cholesterol deposits and pro-inflammatory cytokines play an essential role in the pathogenesis of atherosclerosis, a predominant cause of cardiovascular disease (CVD). Epidemiological evidence has linked periodontal disease (PD) with atherosclerotic CVD. Accordingly, viable periodontal pathogens, including Porphyromonas gingivalis, have been found in atherosclerotic plaques in humans and mice. We aimed to determine whether cholesterol crystals (CHCs) and oral bacteria synergize in the stimulation of human monocytes. Incubation of human monocytes with CHCs induced secretion of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, and IL-8. Moreover, CHCs markedly enhanced secretion of IL-1β by monocytes stimulated with the toll-like receptor (TLR) 4 agonist Escherichia coli lipopolysaccharide (LPS), and the TLR2 agonist Staphylococcus aureus lipoteichoic acid. Notably, CHCs also enhanced IL-1β secretion induced by P. gingivalis LPS and IL-1β secretion induced by whole P. gingivalis bacteria. This enhancement was abrogated by the NLRP3 inflammasome inhibitors Z-YVAD-FMK and glibenclamide. CHCs had no effect on cytokine production induced by P. gingivalis gingipains. Taken together, our findings support that CHCs, via stimulation of NLRP3 inflammasomes, act in synergy with the periodontal pathogen P. gingivalis to promote monocyte secretion of pro-atherogenic cytokines.",
author = "K{\o}llgaard, {Tania Maria Simonsen} and Christian Enevold and Klaus Bendtzen and Hansen, {Peter R.} and Michael Givskov and Palle Holmstrup and Nielsen, {Claus H.}",
year = "2017",
month = feb,
day = "24",
doi = "10.1371/journal.pone.0172773",
language = "English",
volume = "12",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "2",

}

RIS

TY - JOUR

T1 - Cholesterol crystals enhance TLR2-and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis

AU - Køllgaard, Tania Maria Simonsen

AU - Enevold, Christian

AU - Bendtzen, Klaus

AU - Hansen, Peter R.

AU - Givskov, Michael

AU - Holmstrup, Palle

AU - Nielsen, Claus H.

PY - 2017/2/24

Y1 - 2017/2/24

N2 - Cholesterol deposits and pro-inflammatory cytokines play an essential role in the pathogenesis of atherosclerosis, a predominant cause of cardiovascular disease (CVD). Epidemiological evidence has linked periodontal disease (PD) with atherosclerotic CVD. Accordingly, viable periodontal pathogens, including Porphyromonas gingivalis, have been found in atherosclerotic plaques in humans and mice. We aimed to determine whether cholesterol crystals (CHCs) and oral bacteria synergize in the stimulation of human monocytes. Incubation of human monocytes with CHCs induced secretion of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, and IL-8. Moreover, CHCs markedly enhanced secretion of IL-1β by monocytes stimulated with the toll-like receptor (TLR) 4 agonist Escherichia coli lipopolysaccharide (LPS), and the TLR2 agonist Staphylococcus aureus lipoteichoic acid. Notably, CHCs also enhanced IL-1β secretion induced by P. gingivalis LPS and IL-1β secretion induced by whole P. gingivalis bacteria. This enhancement was abrogated by the NLRP3 inflammasome inhibitors Z-YVAD-FMK and glibenclamide. CHCs had no effect on cytokine production induced by P. gingivalis gingipains. Taken together, our findings support that CHCs, via stimulation of NLRP3 inflammasomes, act in synergy with the periodontal pathogen P. gingivalis to promote monocyte secretion of pro-atherogenic cytokines.

AB - Cholesterol deposits and pro-inflammatory cytokines play an essential role in the pathogenesis of atherosclerosis, a predominant cause of cardiovascular disease (CVD). Epidemiological evidence has linked periodontal disease (PD) with atherosclerotic CVD. Accordingly, viable periodontal pathogens, including Porphyromonas gingivalis, have been found in atherosclerotic plaques in humans and mice. We aimed to determine whether cholesterol crystals (CHCs) and oral bacteria synergize in the stimulation of human monocytes. Incubation of human monocytes with CHCs induced secretion of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, and IL-8. Moreover, CHCs markedly enhanced secretion of IL-1β by monocytes stimulated with the toll-like receptor (TLR) 4 agonist Escherichia coli lipopolysaccharide (LPS), and the TLR2 agonist Staphylococcus aureus lipoteichoic acid. Notably, CHCs also enhanced IL-1β secretion induced by P. gingivalis LPS and IL-1β secretion induced by whole P. gingivalis bacteria. This enhancement was abrogated by the NLRP3 inflammasome inhibitors Z-YVAD-FMK and glibenclamide. CHCs had no effect on cytokine production induced by P. gingivalis gingipains. Taken together, our findings support that CHCs, via stimulation of NLRP3 inflammasomes, act in synergy with the periodontal pathogen P. gingivalis to promote monocyte secretion of pro-atherogenic cytokines.

U2 - 10.1371/journal.pone.0172773

DO - 10.1371/journal.pone.0172773

M3 - Journal article

C2 - 28235036

VL - 12

JO - PLoS ONE

JF - PLoS ONE

SN - 1932-6203

IS - 2

M1 - 0172773

ER -

ID: 174599912