Functional role of endogenous CD14 in lipopolysaccharide‐stimulated bone resorption

  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},
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.



Preferential inhibition of cytokine‐stimulated bone resorption by recombinant interferon gamma

  • M. GowenG. NedwinG. Mundy
  • Biology, Medicine
    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • 1986
It is found that interferon‐7 completely abolished bone resorption stimulated by the cytokines interleukin‐1, tumor necrosis factor α and tumor Necrosis factor ß, which may have physiological significance in the local control of trabecular bone volume and bone remodeling.

Role of interleukin-1 and prostaglandin in in vitro bone resorption induced by Actinobacillus actinomycetemcomitans lipopolysaccharide.

Results suggest that both PGE2 and IL-1 participate in Y4 LPS-induced bone resorption in vitro.

Lipopolysaccharide induces up‐regulation of CD14 molecule on monocytes in human whole blood

It is concluded that LPS in whole blood up‐regulates the expression of its own CD14 receptor on monocytes, a phenomenon that could be relevant to the pathogenesis of gram‐negative sepsis.

Actions of recombinant interleukin 1, interleukin 2, and interferon-gamma on bone resorption in vitro.

It is reported here that purified recombinant murine IL 1 is a potent and powerful stimulator of bone resorption in vitro, active over a concentration range of 0.14 to 33 U/ml (1.3 X 10(-12) to 3.1X 10(-10) M).

Osteoblasts mediate interleukin 1 stimulation of bone resorption by rat osteoclasts

Results indicate that IL-1 stimulates bone resorption through a primary action on osteoblasts, which are induced by IL- 1 to transmit a short-range signal that stimulates osteoclastic bone resOrption.

Interactions of lipopolysaccharide with neutrophils in blood via CD14

Findings are consistent with the notion that in blood the observed receptor up‐regulation is in direct response to the action of LPS on neutrophils through CD14 and does not require products from macrophages such as TNF or the production of C5a from the plasma.

Involvement of CD14 in lipopolysaccharide-induced tumor necrosis factor-alpha, IL-6 and IL-8 release by human monocytes and alveolar macrophages.

It is concluded that CD14 is involved in LPS-induced release of TNF-alpha, IL-6, and IL-8 by monocytes and alveolar macrophages and that this receptor appears to be able to recognize LPS directly in the absence of serum.

Upregulation of mouse CD14 expression in Kupffer cells by lipopolysaccharide

Western blot analysis showed that a monoclonal antibody against recombinant mouse CD14 (mCD14), designated rmC5-3, specifically reacted with mouse macrophage cell line J774, but not myeloma cell line

The effects of interferon-gamma and bacterial lipopolysaccharide on CD14 expression in human monocytes.

It is clearly demonstrated that IFN-gamma down-regulates CD14 expression and that LPS following IFN -gamma pretreatment potentiates this effect.

Activation of the adhesive capacity of CR3 on neutrophils by endotoxin: dependence on lipopolysaccharide binding protein and CD14

Enhanced activity of CR3 and other members of the CD11/CD18 family underlies many of the known physiological responses of PMN to LPS and may be a central feature of the in vivo responses ofPMN to endotoxin.