ArticlePloS one2017
Cholesterol crystals enhance TLR2- and TLR4-mediated pro-inflammatory cytokine responses of monocytes to the proatherogenic oral bacterium Porphyromonas gingivalis.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 32 citations in OpenAlex.
- Inhibition of Toll-like Receptors Alters Macrophage Cholesterol Efflux and Foam Cell Formation.International journal of molecular sciences · 2024Article
- Mutanolysin-Digested Peptidoglycan ofInternational journal of molecular sciences · 2023Article
- Integrative analysis of gene and protein expression in atherosclerosis-related pathways modulated by periodontal pathogens. Systematic review.The Japanese dental science review · 2023Review
- The potential role of cholesterol in Parkinson's disease neuropathology: perpetrator or victim.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Review
- New Trends in the Impact of Periodontal Treatment on Early Cardiovascular Diseases Outcomes: Insights and Future Perspectives.Reviews in cardiovascular medicine · 2023Review
- Cracking the intestinal lymphatic system window utilizing oral delivery vehicles for precise therapy.Journal of nanobiotechnology · 2023Review
- PAMPs and DAMPs as the Bridge Between Periodontitis and Atherosclerosis: The Potential Therapeutic Targets.Frontiers in cell and developmental biology · 2022Review
- Innate Receptor Activation Patterns Involving TLR and NLR Synergisms in COVID-19, ALI/ARDS and Sepsis Cytokine Storms: A Review and Model Making Novel Predictions and Therapeutic Suggestions.International journal of molecular sciences · 2021Review
- Inflammasomes in Alveolar Bone Loss.Frontiers in immunology · 2021Review
- Interplay Among the Oral Microbiome, Oral Cavity Conditions, the Host Immune Response, Diabetes Mellitus, and Its Associated-Risk Factors-An Overview.Frontiers in oral health · 2021Review
- Relationship between TNF-α, MMP-8, and MMP-9 levels in gingival crevicular fluid and the subgingival microbiota in periodontal disease.Odontology · 2020Article
- 5,2'-dibromo-2,4',5'-trihydroxydiphenylmethanone attenuates LPS-induced inflammation and ROS production in EA.hy926 cells via HMBOX1 induction.Journal of cellular and molecular medicine · 2019Article
- Porphyromonas gingivalis lipopolysaccharides act exclusively through TLR4 with a resilience between mouse and human.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.