ArticleInfection and immunity2013
A novel class of lipoprotein lipase-sensitive molecules mediates Toll-like receptor 2 activation by Porphyromonas gingivalis.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed.
- The Role ofAntibiotics (Basel, Switzerland) · 2026Review
- Candidalysin InhibitsInternational journal of molecular sciences · 2026Article
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- Porphyromonas gingivalis-derived extracellular vesicles aggravate bone destruction in rheumatoid arthritis by promoting Syk-dependent osteoclastogenesis.International journal of oral science · 2026Article
- Altered microRNA expression correlates with reduced TLR2/4-dependent periodontal inflammation and bone resorption induced by polymicrobial infection.Microbiology spectrum · 2025Article
- Porphyromonas gingivalis outer membrane vesicles divert host innate immunity and promote inflammation via C4' monophosphorylated lipid A.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Lipid a remodeling modulates outer membrane vesicle biogenesis byJournal of bacteriology · 2025Article
- Ozone ultrafine bubble water sterilizes Porphyromonas gingivalis and neutralizes its virulence factors.PloS one · 2025Article
- Recognition ofJournal of oral microbiology · 2025Article
- Targeting host-specific metabolic pathways-opportunities and challenges for anti-infective therapy.Frontiers in molecular biosciences · 2024Review
- Effects of extracellular vesicles derived from oral bacteria on osteoclast differentiation and activation.Scientific reports · 2022Article
- When the infectious environment meets the AD brain.Molecular neurodegeneration · 2022Review
- Airway Prevotella promote TLR2-dependent neutrophil activation and rapid clearance of Streptococcus pneumoniae from the lung.Nature communications · 2022Article
- Periodontitis and cardiometabolic disorders: The role of lipopolysaccharide and endotoxemia.Periodontology 2000 · 2022Review
- Oral and Gut Microbial Dysbiosis and Non-alcoholic Fatty Liver Disease: The Central Role ofFrontiers in medicine · 2022Review
- Overexpression of SGLT2 in the kidney of a P. gingivalis LPS-induced diabetic nephropathy mouse model.BMC nephrology · 2021Article
- Is the oral microbiome a source to enhance mucosal immunity against infectious diseases?NPJ vaccines · 2021Review
- Microbial Lipid A Remodeling Controls Cross-Presentation Efficiency and CD8 T Cell Priming by Modulating Dendritic Cell Function.Infection and immunity · 2021Article
- Immunohistochemical study for the expression of leukocyte adhesion molecules, and FGF23 and ACE2 in P. gingivalis LPS-induced diabetic nephropathy.BMC nephrology · 2021Article
- Serine/Glycine Lipid Recovery in Lipid Extracts From Healthy and Diseased Dental Samples: Relationship to Chronic Periodontitis.Frontiers in oral health · 2021Article
1 more citing papers are in PubMed but not listed here.
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4 authors.
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Abstract
Infection by the chronic periodontitis-associated pathogen Porphyromonas gingivalis activates a Toll-like receptor 2 (TLR2) response that triggers inflammation in the host but also promotes bacterial persistence. Our aim was to define ligands on the surfaces of intact P. gingivalis cells that determine its ability to activate TLR2. Molecules previously reported as TLR2 agonists include lipopolysaccharide (LPS), fimbriae, the lipoprotein PG1828, and phosphoceramides. We demonstrate that these molecules do not comprise the major factors responsible for stimulating TLR2 by whole bacterial cells. First, P. gingivalis mutants devoid of the reported protein agonists, PG1828 and fimbriae, activate TLR2 as strongly as the wild type. Second, two-phase extraction of whole bacteria resulted in a preponderance of TLR2 agonist activity partitioning to the hydrophilic phase, demonstrating that phosphoceramides are not a major TLR2 ligand. Third, analysis of LPS revealed that TLR2 activation is independent of lipid A structural variants. Instead, activation of TLR2 and TLR2/TLR1 by LPS is in large part due to copurifying molecules that are sensitive to the action of the enzyme lipoprotein lipase. Strikingly, intact P. gingivalis bacterial cells treated with lipoprotein lipase were attenuated in their ability to activate TLR2. We propose that a novel class of molecules comprised by lipoproteins constitutes the major determinants that confer to P. gingivalis the ability to stimulate TLR2 signaling.
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