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 Toll-like receptor 2 plays a critical role in the progression of atherosclerosis that is independent of dietary lipids

2008 ◽  
Vol 196 (1) ◽  
pp. 146-154 ◽  
Author(s):  
Xinyan Liu ◽  
Takashi Ukai ◽  
Hiromichi Yumoto ◽  
Michael Davey ◽  
Sulip Goswami ◽  
...  
Keyword(s):  
Critical Role ◽  
Dietary Lipids ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Progression Of Atherosclerosis

1153 – Critical Role of Toll-Like Receptor 2 in Mediating Serotonin Production in Gut

2019 ◽  
Vol 156 (6) ◽  
pp. S-247
Author(s):  
Yun Han Kwon ◽  
Huaqing Wang ◽  
Varun Dewan ◽  
Saad Syed ◽  
Michelle E. Fontes ◽  
...  
Keyword(s):  
Critical Role ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

Critical role of Toll-like receptor 2 inBacteroides fragilis-mediated immune responses in murine peritoneal mesothelial cells

2012 ◽  
Vol 56 (11) ◽  
pp. 782-788 ◽  
Author(s):  
Tae-Hyoun Kim ◽  
Kyung-Bok Lee ◽  
Min-Jung Kang ◽  
Jong-Hwan Park
Keyword(s):  
Immune Responses ◽  
Critical Role ◽  
Mesothelial Cells ◽  
Toll Like Receptor ◽  
Peritoneal Mesothelial Cells ◽  
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 Toll-like receptor 2 plays a critical role in cardiac dysfunction during polymicrobial sepsis*

2010 ◽  
Vol 38 (5) ◽  
pp. 1335-1342 ◽  
Author(s):  
Lin Zou ◽  
Yan Feng ◽  
Yu-Jung Chen ◽  
Rui Si ◽  
Shiqian Shen ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Critical Role ◽  
Polymicrobial Sepsis ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2

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 A Critical Role of Toll-like Receptor 2 in Nerve Injury-induced Spinal Cord Glial Cell Activation and Pain Hypersensitivity

2007 ◽  
Vol 282 (20) ◽  
pp. 14975-14983 ◽  
Author(s):  
Donghoon Kim ◽  
Myung Ah Kim ◽  
Ik-Hyun Cho ◽  
Mi Sun Kim ◽  
Soojin Lee ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Glial Cell ◽  
Nerve Injury ◽  
Cell Activation ◽  
Critical Role ◽  
Toll Like Receptor ◽  
Pain Hypersensitivity ◽  
Glial Cell Activation ◽  
Toll Like Receptor 2

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
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