The bone-resorbing activities in tissue culture of lipopolysaccharides from the bacteria Actinobacillus actinomycetemcomitans, Bacteroides gingivalis and Capnocytophaga ochracea isolated from human mouths

Iino, Yukiko; Hopps, Rosamund M.

doi:10.1016/0003-9969(84)90043-8

Cited by 151 publications

(88 citation statements)

References 19 publications

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“…(11)(12)(13) Indeed, varieties of bacteria-derived molecules have been shown to increase osteoclast differentiation and bone resorption. (16,(36)(37)(38) OCPs, as well as osteoblasts, express functional TLRs, mediating the effects of bacterial products on bone. (15,17,19,22,39,40) Several in vitro cell systems are routinely used to study osteoclast differentiation.…”

Section: Discussionmentioning

confidence: 99%

Differential Contribution of Osteoclast- and Osteoblast-Lineage Cells to CpG-Oligodeoxynucleotide (CpG-ODN) Modulation of Osteoclastogenesis

Amcheslavsky

Hemmi

Akira

et al. 2005

Journal of Bone and Mineral Research

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CpG-ODNs modulate osteoclast differentiation through Toll-like receptor 9 (TLR9). Using TLR9-deficient mice, we found that activation of TLR9 on both osteoclast precursors and osteoblasts mediate the osteoclastogenic effect of CpG-ODN. Osteoclastic TLR9 is more important for this activity.Introduction: Bacterial infections cause pathological bone loss by accelerating differentiation and activation of the osteoclast. A variety of bacteria-derived molecules have been shown to enhance osteoclast differentiation through activation of Toll-like receptors (TLRs). We have shown that CpG-oligodeoxynucleotides (CpG-ODNs), mimicking bacterial DNA and exerting their cellular activities through TLR9, modulate osteoclast differentiation in a complex manner: the ODNs inhibit the activity of the physiological osteoclast differentiation factor RANKL in early osteoclast precursors (OCPs) but markedly stimulate osteoclastogenesis in cells primed by RANKL. Materials and Methods: Osteoclast precursors and osteoblasts from TLR9-deficient (TLR9

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Section: Discussionmentioning

confidence: 99%

Differential Contribution of Osteoclast- and Osteoblast-Lineage Cells to CpG-Oligodeoxynucleotide (CpG-ODN) Modulation of Osteoclastogenesis

Amcheslavsky

Hemmi

Akira

et al. 2005

Journal of Bone and Mineral Research

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“…Not only is LPS abundant in foci of periodontal disease (4,5), but the molecule is known to stimulate bone resorption when added to organ culture (6). The mechanisms by which LPS activates the resorptive process are, however, unknown (2).…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide-stimulated osteoclastogenesis is mediated by tumor necrosis factor via its P55 receptor.

Abu‐Amer¹,

Ross²,

Edwards³

et al. 1997

J. Clin. Invest.

265

251

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Chronic bone infection, as attends periodontitis, is often complicated by severe osteolysis. While LPS is believed to be central to the pathogenesis of the osteolytic lesion, the mechanisms by which this bacteria-derived molecule promotes bone resorption are unknown. We find that LPS induces bone marrow macrophages (BMMs) to express c-src, a protooncogene product that we demonstrate is a specific marker of commitment to the osteoclast phenotype.

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“…Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Peptostreptococcus micros are considered major pathogenic species in destructive periodontal disease (8,21). Many studies have suggested that lipopolysaccharide (LPS) released from the cell walls of gram-negative bacteria or lipoteichoic acid from gram-positive bacteria is associated with the development and progression of periodontal disease (14,30). LPS and lipoteichoic acid activate cells of the innate immune system and thus contribute to inflammatory processes.…”

mentioning

confidence: 99%

DNA from Periodontopathogenic Bacteria Is Immunostimulatory for Mouse and Human Immune Cells

et al. 2003

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Although bacterial DNA (bDNA) containing unmethylated CpG motifs stimulates innate immune cells through Toll-like receptor 9 (TLR-9), its precise role in the pathophysiology of diseases is still equivocal. Here we examined the immunostimulatory effects of DNA extracted from periodontopathogenic bacteria. A major role in the etiology of periodontal diseases has been attributed to Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Peptostreptococcus micros. We therefore isolated DNA from these bacteria and stimulated murine macrophages and human gingival fibroblasts (HGF) in vitro. Furthermore, HEK 293 cells transfected with human TLR-9 were also stimulated with these DNA preparations. We observed that DNA from these pathogens stimulates macrophages and gingival fibroblasts to produce tumor necrosis factor alpha and interleukin-6 in a dose-dependent manner. Methylation of the CpG motifs abolished the observed effects. Activation of HEK 293 cells expressing TLR-9 which were responsive to bDNA but not to lipopolysaccharide confirmed that immunostimulation was achieved by bDNA. In addition, the examined bDNA differed in the ability to stimulate murine macrophages, HGF, and TLR-9-transfected cells. DNA from A. actinomycetemcomitans elicited a potent cytokine response, while DNA from P. gingivalis and P. micros showed lower immunostimulatory activity. Taken together, the results strongly suggest that DNA from A. actinomycetemcomitans, P. gingivalis, and P. micros possesses immunostimulatory properties in regard to cytokine secretion by macrophages and fibroblasts. These stimulatory effects are due to unmethylated CpG motifs within bDNA and differ between distinct periodontopathogenic bacteria strains. Hence, immunostimulation by DNA from A. actinomycetemcomitans, P. gingivalis, and P. micros could contribute to the pathogenesis of periodontal diseases.

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The bone-resorbing activities in tissue culture of lipopolysaccharides from the bacteria Actinobacillus actinomycetemcomitans, Bacteroides gingivalis and Capnocytophaga ochracea isolated from human mouths

Cited by 151 publications

References 19 publications

Differential Contribution of Osteoclast- and Osteoblast-Lineage Cells to CpG-Oligodeoxynucleotide (CpG-ODN) Modulation of Osteoclastogenesis

Differential Contribution of Osteoclast- and Osteoblast-Lineage Cells to CpG-Oligodeoxynucleotide (CpG-ODN) Modulation of Osteoclastogenesis

Lipopolysaccharide-stimulated osteoclastogenesis is mediated by tumor necrosis factor via its P55 receptor.

DNA from Periodontopathogenic Bacteria Is Immunostimulatory for Mouse and Human Immune Cells

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