CpG Oligodeoxynucleotides Modulate the Osteoclastogenic Activity of Osteoblasts via Toll-like Receptor 9

Zou, Wei; Amcheslavsky, Alla; Bar‐Shavit, Zvi

doi:10.1074/jbc.m212473200

Cited by 88 publications

(90 citation statements)

References 61 publications

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“…Consistently higher levels of TNF-␣ were released from BALB/c-derived cells in response to CpG-ODN challenge. We have shown that in cultures containing both osteoclast and osteoblast-lineage cells CpG-ODN induces TNF-␣ in both cell types (9). It was therefore important for the present study that the cultures did not contain osteoblastic or mesenchymal cells.…”

Section: Discussionmentioning

confidence: 99%

“…Bacterial factors have been studied extensively for their ability to activate the innate immune system via Toll-like receptors (TLRs) 1 present on the host immune cells (6,7). Bone cells also express TLRs enabling the bacteria-derived factors to exert their effects on the skeleton (8,9). The most studied bacterial factor in this regard is lipopolysaccharide, recognized by both osteoclast and osteoblast lineage cells via TLR4 (8,9).…”

mentioning

confidence: 99%

“…Bone cells also express TLRs enabling the bacteria-derived factors to exert their effects on the skeleton (8,9). The most studied bacterial factor in this regard is lipopolysaccharide, recognized by both osteoclast and osteoblast lineage cells via TLR4 (8,9). Bacterial DNA has been shown to be a pathogen-derived structure activating the innate immune system via TLR9 (10 -14).…”

mentioning

confidence: 99%

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Toll-like Receptor 9 Regulates Tumor Necrosis Factor-α Expression by Different Mechanisms

Amcheslavsky

Zou

Bar‐Shavit

2004

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Toll-like Receptor 9 Regulates Tumor Necrosis Factor-α Expression by Different Mechanisms

Amcheslavsky

Zou

Bar‐Shavit

2004

Journal of Biological Chemistry

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“…Cell activation Neutrophils (5610 6 cells?mL -1 ) were incubated for 20-30 min with L-NAME (0.1-10 mM) or NAC (0.1-10 mM); chloroquine (1-50 mg?mL -1 ) (enhances endosomal pH and thereby blocks lysomal pathways and used here as a blocker of TLRs signalling) [26] or blocking anti-sense ODN (1-10 mM) and then stimulated with CSE (1.5%), CpG ODN type A (3 mM) or control ODN (5 mM) for 30 min for western blot analysis. For CXCL8 determination 3610 6 cells?mL -1 were incubated for 9 h according to the conditions for Western blot analysis.…”

Section: Isolation Of Neutrophilsmentioning

confidence: 99%

Cigarette smoke induces CXCL8 production by human neutrophils via activation of TLR9 receptor

Mortaz¹,

Adcock²,

Ito³

et al. 2009

European Respiratory Journal

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Chronic obstructive pulmonary disease (COPD) is a major health problem and cigarette smoke is the main risk factor for the development of COPD. The characteristic changes in airway morphology, inflammatory cell infiltration and mediator expression in COPD may result from direct effects of cigarette smoke on airway cells. Toll-like receptors (TLRs) are key elements in pathogen recognition by the host immune system. Although TLRs have been intensely studied in innate immunity and infection, their critical role in noninfectious challenges has only recently emerged.Here we investigate whether cigarette smoke induces TLR9 signalling in human neutrophils. Human neutrophils were isolated from buffy coat and exposed to cigarette smoke extract. The production of CXC chemokine ligand (CXCL)8 was measured as a functional readout and the role of TLR9 signalling was investigated. Cigarette smoke extract induced CXCL8 release via TLR9 activation in neutrophils, which was confirmed in TLR9 stably transfected human embryonic kidney 293 cells. Moreover, cigarette smoke extract upregulated the expression of TLR9 and the upregulated expression was suppressed by N-acetylcysteine.TLR9 mediates cigarette smoke-induced release of CXCL8 and this may contribute to the accumulation of neutrophils and inflammation within the airways of smokers.

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“…Similar to LPS, CpG DNA modulates osteoclastogenesis in bone marrow cell/osteoblast cocultures. Upon TLR-9 ligation, CpG DNA interacts with osteoblastic TLR-9 and elicits intracellular events leading to the increased expression of molecules regulating osteoclastogenesis (59).…”

Section: Bacterial Dnamentioning

confidence: 99%

Bacterial pathogenesis and mediators in apical periodontitis

2007

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Apical periodontitis is a group of inflammatory diseases caused by microorganisms (mainly bacteria) infecting the necrotic root canal system. The pathogenesis of different types of apical periodontitis and even the same type in different individuals is unlikely to follow a stereotyped fashion with regard to the involved bacterial mediators. Disease pathogenesis is rather complex and involves a multitude of bacteria-and host-related factors. This review article discusses the bacterial pathogenesis of acute and chronic apical periodontitis, with the main focus on the bacterial mediators conceivably involved in the different stages of the infectious process, including secreted products (enzymes, exotoxins, N-formyl-methionyl-leucyl-phenylalanine peptides, heat-shock proteins and metabolic end-products) and structural components (lipopolysaccharide, peptidoglycan, lipoteichoic acid, lipoproteins, fimbriae, flagella, outer membrane proteins and vesicles, DNA, and exopolysaccharides). Knowledge of the bacterial factors involved in the pathogenesis of apical periodontitis is important to the understanding of the disease process and to help establishing proper therapeutic measures to inactivate this bacterial "artillery".

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CpG Oligodeoxynucleotides Modulate the Osteoclastogenic Activity of Osteoblasts via Toll-like Receptor 9

Abstract: Regulation of osteoclastogenesis by lipopolysaccharide (LPS) is mediated via its interactions with toll-like

Cited by 88 publications

References 61 publications

Toll-like Receptor 9 Regulates Tumor Necrosis Factor-α Expression by Different Mechanisms

Toll-like Receptor 9 Regulates Tumor Necrosis Factor-α Expression by Different Mechanisms

Cigarette smoke induces CXCL8 production by human neutrophils via activation of TLR9 receptor

Bacterial pathogenesis and mediators in apical periodontitis

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