Macrophage-elicited osteoclastogenesis in response to bacterial stimulation requires Toll-like receptor 2-dependent tumor necrosis factor-alpha production.
about
TLR4 drives the pathogenesis of acquired cholesteatoma by promoting local inflammation and bone destruction.Toll-like receptor 2 and facial motoneuron survival after facial nerve axotomy.Distinct lipid a moieties contribute to pathogen-induced site-specific vascular inflammation.Review: Pathogen-induced inflammation at sites distant from oral infection: bacterial persistence and induction of cell-specific innate immune inflammatory pathways.Porphyromonas gingivalis exacerbates ligature-induced, RANKL-dependent alveolar bone resorption via differential regulation of Toll-like receptor 2 (TLR2) and TLR4.Lysine-specific gingipain promotes lipopolysaccharide- and active-vitamin D3-induced osteoclast differentiation by degrading osteoprotegerinInfection of RANKL-primed RAW-D macrophages with Porphyromonas gingivalis promotes osteoclastogenesis in a TNF-α-independent manner.Absence of interleukin 22 affects the oral microbiota and the progression of induced periapical lesions in murine teeth.TLR signaling that induces weak inflammatory response and SHIP1 enhances osteogenic functions.A Modified Glycosaminoglycan, GM-0111, Inhibits Molecular Signaling Involved in Periodontitis.Macrophage-specific TLR2 signaling mediates pathogen-induced TNF-dependent inflammatory oral bone loss.Importance of TLR2 in early innate immune response to acute pulmonary infection with Porphyromonas gingivalis in miceSerine lipids of Porphyromonas gingivalis are human and mouse Toll-like receptor 2 ligandsExpression of receptor activator of nuclear factor-kappaB ligand by B cells in response to oral bacteria.The role of T cells in osteoporosis, an update.Toll gates to periodontal host modulation and vaccine therapyUnique lipids from a common human bacterium represent a new class of Toll-like receptor 2 ligands capable of enhancing autoimmunityComplementary Tolls in the periodontium: how periodontal bacteria modify complement and Toll-like receptor responses to prevail in the host.Brucella abortus Invasion of Osteocytes Modulates Connexin 43 and Integrin Expression and Induces Osteoclastogenesis via Receptor Activator of NF-κB Ligand and Tumor Necrosis Factor Alpha SecretionEffects of Porphyromonas gingivalis surface-associated material on osteoclast formation.Immunologic environment influences macrophage response to Porphyromonas gingivalis.Role of toll-like receptor 2 in inflammation and alveolar bone loss in experimental peri-implantitis versus periodontitis.Antibiotic administration alleviates the aggravating effect of orthodontic force on ligature-induced experimental periodontitis bone loss in mice.Immune response of macrophages from young and aged mice to the oral pathogenic bacterium Porphyromonas gingivalis.GM-CSF and uPA are required for Porphyromonas gingivalis-induced alveolar bone loss in a mouse periodontitis model.Role of MyD88-dependent and MyD88-independent signaling in Porphyromonas gingivalis-elicited macrophage foam cell formation.Porphyromonas gingivalis lipids inhibit osteoblastic differentiation and function.Aging and contribution of MyD88 and TRIF to expression of TLR pathway-associated genes following stimulation with Porphyromonas gingivalis.Inflammatory response to Porphyromonas gingivalis partially requires interferon regulatory factor (IRF) 3RANKL expression in periodontal disease: where does RANKL come from?Scavenger receptor A is expressed by macrophages in response to Porphyromonas gingivalis, and participates in TNF-alpha expression.Reciprocal effects of Interferon-γ and IL-4 on differentiation to osteoclast-like cells by RANKL or LPS.Macrophage-elicited osteoclastogenesis in response to Brucella abortus infection requires TLR2/MyD88-dependent TNF-α production.Importance of heterogeneity in Porhyromonas gingivalis lipopolysaccharide lipid A in tissue specific inflammatory signalling.Expression of Phospholipase D in Periodontitis and Its Role in the Inflammatory and Osteoclastic Response by Nicotine- and Lipopolysaccharide-Stimulated Human Periodontal Ligament Cells.Peptidoglycan and lipopolysaccharide synergistically enhance bone resorption and osteoclastogenesis.Immunohistochemical and mRNA expression of RANK, RANKL, OPG, TLR2 and MyD88 during apical periodontitis progression in mice.
P2860
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P2860
Macrophage-elicited osteoclastogenesis in response to bacterial stimulation requires Toll-like receptor 2-dependent tumor necrosis factor-alpha production.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
2007年论文
@zh
2007年论文
@zh-cn
name
Macrophage-elicited osteoclast ...... rosis factor-alpha production.
@en
type
label
Macrophage-elicited osteoclast ...... rosis factor-alpha production.
@en
prefLabel
Macrophage-elicited osteoclast ...... rosis factor-alpha production.
@en
P2860
P356
P1476
Macrophage-elicited osteoclast ...... crosis factor-alpha production
@en
P2093
Hiromichi Yumoto
Takashi Ukai
P2860
P304
P356
10.1128/IAI.01241-07
P407
P577
2007-11-12T00:00:00Z