scholarly journals Extracellular vesicles derived from the periodontal pathogen Filifactor alocis induce systemic bone loss through Toll‐like receptor 2

2021 ◽  
Vol 10 (12) ◽  
Author(s):  
Hyun Young Kim ◽  
Min‐Kyoung Song ◽  
Yong Song Gho ◽  
Hong‐Hee Kim ◽  
Bong‐Kyu Choi
Keyword(s):  
Bone Loss ◽  
Extracellular Vesicles ◽  
Periodontal Pathogen ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Filifactor Alocis ◽  
Systemic Bone Loss

scholarly journals Erratum: Corrigendum: Toll-like receptor-2 has a critical role in periodontal pathogen-induced myocardial fibrosis in the pressure-overloaded murine hearts

2017 ◽  
Vol 40 (2) ◽  
pp. 212-212
Author(s):  
Makoto Kaneko ◽  
Jun-ichi Suzuki ◽  
Norio Aoyama ◽  
Ryo Watanabe ◽  
Asuka Yoshida ◽  
...  
Keyword(s):  
Myocardial Fibrosis ◽  
Critical Role ◽  
Periodontal Pathogen ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

Toll-like receptor-2 has a critical role in periodontal pathogen-induced myocardial fibrosis in the pressure-overloaded murine hearts

2016 ◽  
Vol 40 (2) ◽  
pp. 110-116 ◽  
Author(s):  
Makoto Kaneko ◽  
Jun-ichi Suzuki ◽  
Norio Aoyama ◽  
Ryo Watanabe ◽  
Asuka Yoshida ◽  
...  
Keyword(s):  
Myocardial Fibrosis ◽  
Critical Role ◽  
Periodontal Pathogen ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

scholarly journals Signaling by Toll-Like Receptor 2 and 4 Agonists Results in Differential Gene Expression in Murine Macrophages

2001 ◽  
Vol 69 (3) ◽  
pp. 1477-1482 ◽  
Author(s):  
Matthew Hirschfeld ◽  
Janis J. Weis ◽  
Vladimir Toshchakov ◽  
Cindy A. Salkowski ◽  
M. Joshua Cody ◽  
...  
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Periodontal Pathogen ◽  
Agonist Activity ◽  
Toll Like Receptor ◽  
Inflammatory Gene Expression ◽  
Murine Macrophages ◽  
Tlr4 Agonist ◽  
Differential Gene ◽  
Toll Like Receptor 2

ABSTRACT Lipopolysaccharide (LPS) derived from the periodontal pathogenPorphyromonas gingivalis has been reported to differ structurally and functionally from enterobacterial LPS. These studies demonstrate that in contrast to protein-free enterobacterial LPS, a similarly purified preparation of P. gingivalis LPS exhibited potent Toll-like receptor 2 (TLR2), rather than TLR4, agonist activity to elicit gene expression and cytokine secretion in murine macrophages and transfectants. More importantly, TLR2 stimulation by this P. gingivalis LPS preparation resulted in differential expression of a panel of genes that are normally induced in murine macrophages by Escherichia coli LPS. These data suggest that (i) P. gingivalis LPS does not signal through TLR4 and (ii) signaling through TLR2 and through TLR4 differs quantitatively and qualitatively. Our data support the hypothesis that the shared signaling pathways elicited by TLR2 and by TLR4 agonists must diverge in order to account for the distinct patterns of inflammatory gene expression.

scholarly journals Mangiferin alleviates experimental peri-implantitis via suppressing interleukin-6 production and Toll-like receptor 2 signaling pathway

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Hao Li ◽  
Zhiyong Chen ◽  
Xinghua Zhong ◽  
Jiaquan Li ◽  
Wei Li
Keyword(s):  
Bone Loss ◽  
Western Blot ◽  
Inflammatory Infiltrate ◽  
Alveolar Bone ◽  
Pcr Analysis ◽  
Micro Ct ◽  
Toll Like Receptor ◽  
Qrt Pcr ◽  
Toll Like Receptor 2 ◽  
Tlr2 Signaling

Abstract Background TLR2 (Toll-like receptor 2) signaling and its downstream proinflammatory cytokines are considered to be important in the progression of peri-implantitis. A natural medicine, mangiferin has exhibited modulatory effect on TLR2 signaling and anti-inflammatory effects on different diseases. The objective of the present study is to investigate the effect of mangiferin on peri-implantitis and the potential mechanisms by administering this drug to an experimental peri-implantitis mouse model. Methods Maxillary left first, second, and third molars of mice were extracted, and dental implants were placed in the region of the maxillary left second molars. Then, peri-implantitis was induced by tying ligatures around implants, and mangiferin was given orally to the mice. After 6-week mangiferin treatment, bone loss around the implants was detected using micro-computerized tomography (micro-CT). Alveolar bone and inflammatory infiltrate in peri-implant tissues were examined using hematoxylin and eosin (H&E) staining. Production of interleukin-6 (IL6), a TLR2 downstream proinflammatory cytokine, in the tissue surrounding implants was measured using quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) analysis. IL6 protein expression and TLR2 signaling pathway activation in peri-implant tissues were detected using western blot analysis. Results Micro-CT demonstrated reduced bone loss in peri-implantitis upon mangiferin administration. Additionally, H&E staining showed more alveolar bone and less inflammatory infiltrate in peri-implant tissues after mangiferin application. Moreover, qRT-PCR analysis demonstrated lower levels of IL6 gene expression, and western blot analysis showed decreased protein expression of IL6 and TLR2, and suppressed phosphorylation of TLR2 downstream nuclear factor-κB, p38 mitogen-activated protein kinase, and c-Jun N-terminal kinase after mangiferin treatment. Conclusions These results suggest the suppressive effect of mangiferin on bone damage and inflammatory infiltrate in peri-implantitis. These therapeutic effects may be associated with inhibited IL6 production and reduced TLR2 signaling activation in peri-implant tissues.

scholarly journals Serine Lipids of Porphyromonas gingivalis Are Human and Mouse Toll-Like Receptor 2 Ligands

2013 ◽  
Vol 81 (9) ◽  
pp. 3479-3489 ◽  
Author(s):  
Robert B. Clark ◽  
Jorge L. Cervantes ◽  
Mark W. Maciejewski ◽  
Vahid Farrokhi ◽  
Reza Nemati ◽  
...  
Keyword(s):  
Cell Activation ◽  
Inflammatory Responses ◽  
Periodontal Pathogen ◽  
Toll Like Receptor ◽  
Dendritic Cell Activation ◽  
Content Type ◽  
Hek Cells ◽  
Toll Like Receptor 2

ABSTRACTThe total cellular lipids ofPorphyromas gingivalis, a known periodontal pathogen, were previously shown to promote dendritic cell activation and inhibition of osteoblasts through engagement of Toll-like receptor 2 (TLR2). The purpose of the present investigation was to fractionate all lipids ofP. gingivalisand define which lipid classes account for the TLR2 engagement, based on bothin vitrohuman cell assays andin vivostudies in mice. Specific serine-containing lipids ofP. gingivalis, called lipid 654 and lipid 430, were identified in specific high-performance liquid chromatography fractions as the TLR2-activating lipids. The structures of these lipids were defined using tandem mass spectrometry and nuclear magnetic resonance methods.In vitro, both lipid 654 and lipid 430 activated TLR2-expressing HEK cells, and this activation was inhibited by anti-TLR2 antibody. In contrast, TLR4-expressing HEK cells failed to be activated by either lipid 654 or lipid 430. Wild-type (WT) or TLR2-deficient (TLR2−/−) mice were injected with either lipid 654 or lipid 430, and the effects on serum levels of the chemokine CCL2 were measured 4 h later. Administration of either lipid 654 or lipid 430 to WT mice resulted in a significant increase in serum CCL2 levels; in contrast, the administration of lipid 654 or lipid 430 to TLR2−/−mice resulted in no increase in serum CCL2. These results thus identify a new class of TLR2 ligands that are produced byP. gingivalisthat likely play a significant role in mediating inflammatory responses both at periodontal sites and, potentially, in other tissues where these lipids might accumulate.

scholarly journals Identification of a Gingipain-Sensitive Surface Ligand of Porphyromonas gingivalis That Induces Toll-Like Receptor 2- and 4-Independent NF-κB Activation in CHO Cells

2009 ◽  
Vol 77 (10) ◽  
pp. 4414-4420 ◽  
Author(s):  
Koki Haruyama ◽  
Atsutoshi Yoshimura ◽  
Mariko Naito ◽  
Mami Kishimoto ◽  
Mikio Shoji ◽  
...  
Keyword(s):  
Porphyromonas Gingivalis ◽  
Periodontal Pathogen ◽  
Mass Spectrometry Analysis ◽  
Deletion Mutants ◽  
Toll Like Receptor ◽  
Spectrometry Analysis ◽  
Flight Mass Spectrometry ◽  
Virulence Potential ◽  
A Cell ◽  
Toll Like Receptor 2

ABSTRACT Porphyromonas gingivalis is a major periodontal pathogen that has the pathogenic proteinases Arg-specific gingipain and Lys-specific gingipain. We previously found that a cell surface component on P. gingivalis is able to induce Toll-like receptor 2 (TLR2)- and TLR4-independent signaling in 7.19 cells and that this component can be degraded by gingipains. In this study, we purified this component from the P. gingivalis gingipain-null mutant KDP136 and obtained two candidate proteins. Matrix-assisted laser desorption ionization-time-of-flight mass spectrometry analysis showed that the proteins, with molecular masses of 123 and 43 kDa, were encoded by PGN_0748 and PGN_0728 (pgm6), respectively, in the P. gingivalis ATCC 33277 genome sequence. The PGN_0748-encoded protein, which we refer to as gingipain-sensitive ligand A (GslA), reacted with antiserum that could effectively inhibit the activity of KDP136 to induce NF-κB activation in 7.19 cells, but Pgm6 did not. To further determine what protein is responsible for the NF-κB activation, we constructed gslA, pgm6, and pgm6 pgm7 deletion mutants from KDP136. When 7.19 cells were exposed to those mutants, the gslA deletion mutant did not induce NF-κB activation, whereas the pgm6 and pgm6 pgm7 deletion mutants did. Furthermore, NF-κB activation in 7.19 cells induced by KDP136 was partially inhibited by antiserum against a recombinant protein expressed from the 5′-terminal third of gslA. These results indicate that GslA is one of the factors that induce NF-κB activation in 7.19 cells. Interestingly, the gslA gene was present in four of seven P. gingivalis strains tested. This restricted distribution might be associated with the virulence potential of each strain.

scholarly journals Lipopolysaccharidefrom the Periodontal Pathogen Porphyromonas gingivalisPrevents Apoptosis of HL60-Derived Neutrophils InVitro

2003 ◽  
Vol 71 (12) ◽  
pp. 7232-7235 ◽  
Author(s):  
D. A Murray ◽  
J. M. A. Wilton
Keyword(s):  
Porphyromonas Gingivalis ◽  
Interleukin 10 ◽  
Periodontal Pathogen ◽  
Toll Like Receptor ◽  
Inhibiting Effect ◽  
Periodontal Inflammation ◽  
Toll Like Receptor 2

ABSTRACT Lipopolysaccharide (LPS) from Porphyromonas gingivalis prevented apoptosis of HL60-derived neutrophils, which could not be restored upon the addition of interleukin-10. Signaling of P. gingivalis LPS through Toll-like receptor 2 (TLR2), not TLR4, may account for the inhibiting effect of P. gingivalis LPS on apoptosis and provide a mechanism for the development of destructive periodontal inflammation.

Sign in / Sign up

Export Citation Format

Share Document