Functional role of endogenous CD14 in lipopolysaccharide‐stimulated bone resorption

@article{Amano1997FunctionalRO,
  title={Functional role of endogenous CD14 in lipopolysaccharide‐stimulated bone resorption},
  author={Shigeru Amano and Kazutake Kawakami and Hiroyoshi Iwahashi and Shigeo Kitano and Shigemasa Hanazawa},
  journal={Journal of Cellular Physiology},
  year={1997},
  volume={173}
}
Lipopolysaccharide (LPS) is a bacterial cell component that plays multifunctional roles in inflammatory reactions, and one of these roles is that of a powerful stimulator of bone resorption. However, the mechanism by which LPS stimulates bone resorption is not yet understood. In the present study, we show, by using mouse embryonic calvarial cells, that endogenous CD14 and interleukin‐1β (IL‐1β) play an important role in the LPS‐mediated bone resorption and that interferon‐γ (IFN‐γ)functions as… 

Signal transduction system for interleukin-6 synthesis stimulated by lipopolysaccharide in human osteoblasts.

  • A. KondoY. KoshiharaA. Togari
  • Biology, Medicine
    Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research
  • 2001
The findings of the present study suggest that the LPS receptor CD14, existent in human osteoblastic cells, and IL-6 synthesis in response to LPS probably occur viaCD14, p38 MAPK, and MAP kinase/extracellular-regulated kinase kinase (MEK), leading to the transcriptional activation of AP-1 in human bone resorption cells.

Regulation of bone sialoprotein (BSP) gene transcription by lipopolysaccharide

It is shown that LPS suppresses BSP gene transcription through PKA and tyrosine kinase‐dependent pathways and that the LPS effects are mediated through CRE and FRE elements in the proximal B SP gene promoter.

Gene Expression of Osteoclast Differentiation Factor Is Induced by Lipopolysaccharide in Mouse Osteoblasts Via Toll-Like Receptors1

The results indicate that ODF gene expression is directly increased in osteoblasts by LPS treatment via TLR, and this pathway may play an important role in the pathogenesis of LPS-mediated bone disorders, such as periodontitis.

Involvement of prostaglandin E2 and interleukin-1 alpha in the differentiation and survival of osteoclasts induced by lipopolysaccharide from Actinobacillus actinomycetemcomitans Y4.

It is demonstrated that LPS from periodontopathic bacterium Actinobacillus actinomycetemcomitans Y4 (Y4 LPS) stimulated osteoclast formation in mouse bone marrow culture systems and supported the survival of osteoclasts, suggesting that the increased PGE2 and IL-1 alpha synthesis by bone marrow cells may play an important role in the differentiation and survival ofbone marrow cells.

JAK 2 / STAT 5 signaling in the lipopolysaccharide ( LPS )-induced inhibition of osteoblast differentiation

It is shown that LPS inhibits osteoblast differentiation by suppressing the expression of ALP, PINP and RUNX2, all of which are essential for the osteobasts differentiation, in a JAK2/STAT5 signaling-dependent manner.

Lipopolysaccharide from Prevotella nigrescens stimulates osteoclastogenesis in cocultures of bone marrow mononuclear cells and primary osteoblasts.

It is demonstrated that P. nigrescens lipopolysaccharide stimulates osteoclastogenesis in the coculture system by decreasing the production of OPG and increasing theProduction of TGF-beta and PGE2, which may cause alveolar bone resorption in periodontal diseases.

Inhibition of Osteoblastic Cell Differentiation by Lipopolysaccharide Extract from Porphyromonas gingivalis

Results indicate that P-LPS inhibits osteoblastic-cell differentiation and suggest that LPS-induced bone resorption in periodontal disease may be mediated by effects on osteobastic as well as osteoclastic cells.

Peri-Implant Crestal Bone Loss: A Putative Mechanism

The hypothesis that bacterial endotoxins upregulate enhanced mediators of osteoclastogenesis in resident cells found in the healthy peri-implant compartment is supported and that the local synergistic action of cytokines secreted by such cells results in the genesis of resorptively active osteoclasts.

Lipopolysaccharide enhances the production of nicotine-induced prostaglandin E2 by an increase in cyclooxygenase-2 expression in osteoblasts.

LPS enhances the production of nicotine-induced PGE(2) by an increase in COX-2 expression in osteoblasts, which decreases ALPase activity and increases M-CSF expression, which suggests tobacco smoking might be an important risk factor for the development and severity of periodontitis.

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