ArticleInfection and immunity2002
Porphyromonas gingivalis lipopolysaccharide is both agonist and antagonist for p38 mitogen-activated protein kinase activation.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 107 citations in OpenAlex.
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- Enhancing attachment of human gingival fibroblasts to periodontally compromised teeth: A comparative analysis of hyaluronic acid, EDTA, enamel matrix derivatives.The Saudi dental journal · 2023Article
- Oral and Gut Microbial Dysbiosis and Non-alcoholic Fatty Liver Disease: The Central Role ofFrontiers in medicine · 2022Review
- Is the oral microbiome a source to enhance mucosal immunity against infectious diseases?NPJ vaccines · 2021Review
- Lipopolysaccharide- TLR-4 Axis regulates Osteoclastogenesis independent of RANKL/RANK signaling.BMC immunology · 2021Article
- Ginsenoside Rb3 Inhibits Pro-Inflammatory Cytokines via MAPK/AKT/NF-κB Pathways and Attenuates Rat Alveolar Bone Resorption in Response toMolecules (Basel, Switzerland) · 2020Article
- Roles of Porphyromonas gingivalis and its virulence factors in periodontitis.Advances in protein chemistry and structural biology · 2020Review
- Activation of Notch-1 in oral epithelial cells by P. gingivalis triggers the expression of the antimicrobial protein PLAMucosal immunology · 2018Article
- Resistance of MMP9 and TIMP1 to endotoxin tolerance.Pathogens and disease · 2015Article
- Effects of Intravenous Injection of Porphyromonas gingivalis on Rabbit Inflammatory Immune Response and Atherosclerosis.Mediators of inflammation · 2015Article
- Scratching the surface - tobacco-induced bacterial biofilms.Tobacco induced diseases · 2015Article
- Hemoglobin receptor protein from Porphyromonas gingivalis induces interleukin-8 production in human gingival epithelial cells through stimulation of the mitogen-activated protein kinase and NF-κB signal transduction pathways.Infection and immunity · 2014Article
- TLR signaling that induces weak inflammatory response and SHIP1 enhances osteogenic functions.Bone research · 2014Article
- Porphyromonas gingivalis lipopolysaccharide activates canonical Wnt/β-catenin and p38 MAPK signalling in stem cells from the apical papilla.Inflammation · 2013Article
- Article
- Free lipid A isolated from Porphyromonas gingivalis lipopolysaccharide is contaminated with phosphorylated dihydroceramide lipids: recovery in diseased dental samples.Infection and immunity · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Lipopolysaccharide (LPS) is a key inflammatory mediator. It has been proposed to function as an important molecule that alerts the host of potential bacterial infection. Although highly conserved, LPS contains important structural differences among different bacterial species that can significantly alter host responses. For example, LPS obtained from Porphyromonas gingivalis, an etiologic agent for periodontitis, evokes a highly unusual host cell response. Human monocytes respond to this LPS by the secretion of a variety of different inflammatory mediators, while endothelial cells do not. In addition, P. gingivalis LPS inhibits endothelial cell expression of E-selectin and interleukin 8 (IL-8) induced by other bacteria. In this report the ability of P. gingivalis LPS to activate p38 mitogen-activated protein (MAP) kinase was investigated. It was found that p38 MAP kinase activation occurred in response to P. gingivalis LPS in human monocytes. In contrast, no p38 MAP kinase activation was observed in response to P. gingivalis LPS in human endothelial cells or CHO cells transfected with human Toll-like receptor 4 (TLR-4). In addition, P. gingivalis LPS was an effective inhibitor of Escherichia coli-induced p38 MAP kinase phosphorylation in both endothelial cells and CHO cells transfected with human TLR-4. These data demonstrate that P. gingivalis LPS activates the LPS-associated p38 MAP kinase in monocytes and that it can be an antagonist for E. coli LPS activation of p38 MAP kinase in endothelial and CHO cells. These data also suggest that although LPS is generally considered a bacterial component that alerts the host to infection, LPS from P. gingivalis may selectively modify the host response as a means to facilitate colonization.
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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.