ArticleMolecular immunology2009
Requirement of TLR4 and CD14 in dendritic cell activation by Hemagglutinin B from Porphyromonas gingivalis.
Article in Molecular immunology, 2009. 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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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
22 citing papers in PubMed, 35 citations in OpenAlex.
- Review
- Enhanced dual function of osteoclast precursors following calvarial Porphyromonas gingivalis infection.Journal of periodontal research · 2020Article
- Mucosal Immunity and the FOXO1 Transcription Factors.Frontiers in immunology · 2019Review
- Synthesis and Evaluation of QS-21-Based Immunoadjuvants with a Terminal-Functionalized Side Chain Incorporated in the West Wing Trisaccharide.The Journal of organic chemistry · 2016Article
- Role of Porphyromonas gingivalis HmuY in Immunopathogenesis of Chronic Periodontitis.Mediators of inflammation · 2016Review
- Innate Immune Response of Human Embryonic Stem Cell-Derived Fibroblasts and Mesenchymal Stem Cells to Periodontopathogens.Stem cells international · 2016Article
- Liver X receptors contribute to periodontal pathogen-elicited inflammation and oral bone loss.Molecular oral microbiology · 2015Article
- The negative feedback regulation of microRNA-146a in human periodontal ligament cells after Porphyromonas gingivalis lipopolysaccharide stimulation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 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
- Dendritic cell activation and maturation induced by recombinant calreticulin fragment 39-272.International journal of clinical and experimental medicine · 2015Article
- Porphyromonas gingivalis exacerbates ligature-induced, RANKL-dependent alveolar bone resorption via differential regulation of Toll-like receptor 2 (TLR2) and TLR4.Infection and immunity · 2014Article
- In vivo immunotoxicity of SiO2@(Y0.5Gd0.45Eu0.05)2O3 as dual-modality nanoprobes.International journal of molecular sciences · 2014Article
- Immuno-pathogenesis of Periodontal Disease: Current and Emerging Paradigms.Current oral health reports · 2014Article
- Inflammatory response to Porphyromonas gingivalis partially requires interferon regulatory factor (IRF) 3.Innate immunity · 2014Article
- 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
- Synthesis of QS-21-based immunoadjuvants.The Journal of organic chemistry · 2013Article
- Role of MyD88-dependent and MyD88-independent signaling in Porphyromonas gingivalis-elicited macrophage foam cell formation.Molecular oral microbiology · 2013Article
- Vitamin C Up-regulates Expression of CD80, CD86 and MHC Class II on Dendritic Cell Line, DC-1 Via the Activation of p38 MAPK.Immune network · 2012Article
- Inhibition of GSK3 abolishes bacterial-induced periodontal bone loss in mice.Molecular medicine (Cambridge, Mass.) · 2012Article
- Pattern recognition receptors in equine endotoxaemia and sepsis.Equine veterinary journal · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Porphyromonas gingivalis is a Gram-negative anaerobic bacterium that is one of the causative agents of chronic adult periodontal disease. Among the potential virulence factors of P. gingivalis are the hemagglutinins. Recombinant Hemagglutinin B (rHagB) from P. gingivalis has been shown to activate the immune system by inducing specific antibodies that protect against experimental periodontal bone loss following P. gingivalis infection. Since different microbial products can stimulate dendritic cells (DC) through Toll-like receptors (TLRs), subsequently leading to T cell activation and antibody production, we wanted to investigate the immunostimulatory effect of rHagB on DC and the role of TLR signaling in this process. Using an endotoxin free rHagB preparation, our results show that stimulation of murine bone marrow-derived DC with rHagB leads to upregulation of the costimulatory molecules CD86 and CD40, activation of p38 and ERK MAP kinases, transcription factors NF-kappaB, CREB and IRF-3 and the production of IL-6, TNF-alpha, IL-12p40 and to a lesser extent IL-10 and IFN-beta. This activation process was absolutely dependent on TLR4 and CD14. While upregulation of CD86 was independent of the adaptor molecule MyD88, CD40 upregulation and optimal cytokine (IL-6, TNF-alpha, IL-12p40, IL-10 and IFN-beta) production required both MyD88 and TRIF molecules. These results are of importance since they are the first to provide insights into the interaction of rHagB with DC and TLRs. The information from this study will aid in the design of effective vaccines strategies against chronic adult periodontal disease.
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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.