ArticleMolecular oral microbiology2013
Role of MyD88-dependent and MyD88-independent signaling in Porphyromonas gingivalis-elicited macrophage foam cell formation.
Article in Molecular oral microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- A systematic review of the impact of Porphyromonas gingivalis on foam cell formation: Implications for the role of periodontitis in atherosclerosis.BMC oral health · 2023Pooled it
- Bibliometric research on analysis of links between periodontitis and cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Article
- Review
- Infection and atherosclerosis: TLR-dependent pathways.Cellular and molecular life sciences : CMLS · 2020Review
- Review
- Signaling events in pathogen-induced macrophage foam cell formation.Pathogens and disease · 2016Article
- The GroEL protein of Porphyromonas gingivalis regulates atherogenic phenomena in endothelial cells mediated by upregulating toll-like receptor 4 expression.American journal of translational research · 2016Article
- Liver X receptors contribute to periodontal pathogen-elicited inflammation and oral bone loss.Molecular oral microbiology · 2015Article
- Aging and contribution of MyD88 and TRIF to expression of TLR pathway-associated genes following stimulation with Porphyromonas gingivalis.Journal of periodontal research · 2015Article
- Infectious burden and atherosclerosis: A clinical issue.World journal of clinical cases · 2014Review
- LPS-stimulated inflammatory environment inhibits BMP-2-induced osteoblastic differentiation through crosstalk between TLR4/MyD88/NF-κB and BMP/Smad signaling.Stem cells and development · 2014Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Clinical studies and experimental modeling identify a potential link between periodontal disease and periodontal pathogens such as Porphyromonas gingivalis and atherosclerosis and formation of macrophage foam cells. Toll-like receptors and molecules governing their intracellular signaling pathways such as MyD88 play roles in atherosclerosis, as well as host response to P. gingivalis. The aim of this study was to define roles of MyD88 and TRIF during macrophage foam cell formation in response to P. gingivalis. In the presence of human low-density lipoprotein (LDL) mouse bone-marrow-derived macrophages (BMφ) cultured with P. gingivalis responded with significant reduction in tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). The BMφ stained strongly with oil red O, regardless of whether bacterial challenge occurred concurrent with or before LDL treatment. Heat-killed P. gingivalis stimulated foam cell formation in a similar way to live bacteria. The BMφ from MyD88-knockout and Lps2 mice revealed a significant role for MyD88, and a minor role for TRIF in P. gingivalis-elicited foam cell formation. Porphyromonas gingivalis-elicited TNF-α and IL-6 were affected by MyD88 ablation and to a lesser extent by TRIF status. These data indicate that LDL affects the TNF-α and IL-6 response of macrophages to P. gingivalis challenge and that MyD88 and TRIF play important roles in P. gingivalis-elicited foam cell formation.
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Registered trials
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.