ArticleInfection and immunity2012
Free lipid A isolated from Porphyromonas gingivalis lipopolysaccharide is contaminated with phosphorylated dihydroceramide lipids: recovery in diseased dental samples.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- Sphingolipid Metabolism in Oral Diseases: Pathogenic Mechanisms, Biomarkers, and Therapeutic Opportunities.Biomedicines · 2026Review
- Association between lipid-A-producing oral bacteria of different potency and fractional exhaled nitric oxide in a Norwegian population-based adult cohort.Journal of translational medicine · 2023Article
- Complete Structural Elucidation of Monophosphorylated Lipid A by CID Fragmentation of Protonated Molecule and Singly Charged Sodiated Adducts.Journal of the American Society for Mass Spectrometry · 2023Article
- Periodontitis and cardiometabolic disorders: The role of lipopolysaccharide and endotoxemia.Periodontology 2000 · 2022Review
- Exposure toJournal of clinical medicine · 2020Article
- Glycine Lipids of Porphyromonas gingivalis Are Agonists for Toll-Like Receptor 2.Infection and immunity · 2020Article
- Activation of Toll-like receptor 2 induces BScientific reports · 2019Article
- Pathogenesis of Important Virulence Factors ofFrontiers in cellular and infection microbiology · 2019Review
- Are Sphingolipids and Serine Dipeptide Lipids Underestimated Virulence Factors of Porphyromonas gingivalis?Infection and immunity · 2018Review
- Importance of heterogeneity inJournal of oral microbiology · 2018Review
- Macrophage Polarization in Chronic Inflammatory Diseases: Killers or Builders?Journal of immunology research · 2018Review
- Porphyromonas gingivalis lipopolysaccharides act exclusively through TLR4 with a resilience between mouse and human.Scientific reports · 2017Article
- Phosphoglycerol dihydroceramide, a distinctive ceramide produced by Porphyromonas gingivalis, promotes RANKL-induced osteoclastogenesis by acting on non-muscle myosin II-A (Myh9), an osteoclast cell fusion regulatory factor.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017Article
- Genes Contributing toFrontiers in cellular and infection microbiology · 2017Article
- Synthesis of Sphingolipids Impacts Survival ofFrontiers in microbiology · 2016Article
- Different effects of Porphyromonas gingivalis lipopolysaccharide and TLR2 agonist Pam3CSK4 on the adhesion molecules expression in endothelial cells.Odontology · 2015Article
- Distinct gene signatures in aortic tissue from ApoE-/- mice exposed to pathogens or Western diet.BMC genomics · 2014Article
- Biologic activity of porphyromonas endodontalis complex lipids.Journal of endodontics · 2014Article
- Distinct lipid a moieties contribute to pathogen-induced site-specific vascular inflammation.PLoS pathogens · 2014Article
- Serine lipids of Porphyromonas gingivalis are human and mouse Toll-like receptor 2 ligands.Infection and immunity · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Recent reports indicate that Porphyromonas gingivalis mediates alveolar bone loss or osteoclast modulation through engagement of Toll-like receptor 2 (TLR2), though the factors responsible for TLR2 engagement have yet to be determined. Lipopolysaccharide (LPS) and lipid A, lipoprotein, fimbriae, and phosphorylated dihydroceramides of P. gingivalis have been reported to activate host cell responses through engagement of TLR2. LPS and lipid A are the most controversial in this regard because conflicting evidence has been reported concerning the capacity of P. gingivalis LPS or lipid A to engage TLR2 versus TLR4. In the present study, we first prepared P. gingivalis LPS by the Tri-Reagent method and evaluated this isolate for contamination with phosphorylated dihydroceramide lipids. Next, the lipid A prepared from this LPS was evaluated for the presence of phosphorylated dihydroceramide lipids. Finally, we characterized the lipid A by the matrix-assisted laser desorption ionization mass spectrometry (MALDI-MS) and electrospray-MS methods in order to quantify recovery of lipid A in lipid extracts from diseased teeth or subgingival plaque samples. Our results demonstrate that both the LPS and lipid A derived from P. gingivalis are contaminated with phosphorylated dihydroceramide lipids. Furthermore, the lipid extracts derived from diseased teeth or subgingival plaque do not contain free lipid A constituents of P. gingivalis but contain substantial amounts of phosphorylated dihydroceramide lipids. Therefore, the free lipid A of P. gingivalis is not present in measurable levels at periodontal disease sites. Our results also suggest that the TLR2 activation of host tissues attributed to LPS and lipid A of P. gingivalis could actually be mediated by phosphorylated dihydroceramides.
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Registered trials
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