Soluble CD14‐Dependent Intercellular Adhesion Molecule‐1 Induction by <i>Porphyromonas gingivalis</i> Lipopolysaccharide in Human Gingival Fibroblasts

Masaka, Tamami; Hayashi, Joichiro; Ishikawa, Isao

doi:10.1902/jop.1999.70.7.772

Cited by 11 publications

(7 citation statements)

References 48 publications

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“…The anti‐CD14 antibody experiments suggest that the CD14 pathway may play a crucial role in the mechanism of P. gingivalis ‐mediated chemokine induction. Previous studies have also demonstrated that human gingival fibroblasts were activated by P. gingivalis through a CD14‐dependent mechanism [14, 42]. In our study, membrane CD14 expressed on endothelial cells [43] and/or soluble CD14 in culture medium were considered to be involved in the stimulatory effect of P. gingivalis .…”

Section: Discussionsupporting

confidence: 53%

CD14‐Mediated Induction of Interleukin‐8 and Monocyte Chemoattractant Protein‐1 by a Heat‐Resistant Constituent of Porphyromonas gingivalis in Endothelial Cells

Song¹,

Maeno

Yoshiie³

et al. 2002

Scand J Immunol

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Viable and inactivated Porphyromonas gingivalis dose-dependently induced interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) secretion in human umbilical vein endothelial cells (HUVECs). The inactivated P. gingivalis, in comparison with viable bacteria, tended to enhance the production of both chemokines more strongly. The production of MCP-1 protein began increasing immediately after stimulation by P. gingivalis, and there was a nearly linear increase from 0 to 8 h of incubation, whereas IL-8 production showed a linear increase between 4 and 12 h of incubation. The IL-8 and MCP-1 mRNA expressions in HUVECs as determined by reverse transcriptase-polymerase chain reaction (RT-PCR) or Quantikine mRNA colorimetric quantification kits were found to be enhanced by P. gingivalis. Furthermore, the time courses of IL-8 and MCP-1 mRNA expressions were in accordance with those of protein production. Addition of polymyxin B or boiling did not weaken the stimulatory effect of P. gingivalis, which inhibited the effect of Escherichia coli lipopolysaccharide (E. coli LPS) and tumour necrosis factor-a (TNF-a), respectively. In contrast, the induction of IL-8 and MCP-1 by P. gingivalis was significantly reduced by anti-CD14 antibody. Our results suggest that some heatstable component of P. gingivalis, including LPS, may be responsible for the induction of IL-8 and MCP-1 in HUVECs by a CD14-dependent mechanism. These effects might be involved in the accumulation and activation of neutrophils and monocytes at an early stage of the periodontal pathogenesis.

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Section: Discussionsupporting

confidence: 53%

CD14‐Mediated Induction of Interleukin‐8 and Monocyte Chemoattractant Protein‐1 by a Heat‐Resistant Constituent of Porphyromonas gingivalis in Endothelial Cells

Song¹,

Maeno

Yoshiie³

et al. 2002

Scand J Immunol

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“…LPS from periodontopathic bacteria induced secretion of inflammatory cytokines by human polymorphonuclear leukocytes [Yoshimura et al, 1997]. P. gingivalis LPS induces intercellular adhesion molecule‐1 (ICAM‐1) expression in human gingival fibroblasts in a soluble CD14 dependent manner [Masaka et al, 1999]. These findings suggest that LPS is one of the crucial factors in periodontal diseases.…”

Section: Discussionmentioning

confidence: 99%

Regulation of bone sialoprotein (BSP) gene transcription by lipopolysaccharide

Kato

Nakayama

Nakajima

et al. 2005

J of Cellular Biochemistry

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Lipopolysaccharide (LPS) is a major mediator of inflammatory responses in periodontal disease that inhibits bone formation and stimulates bone resorption. To determine the molecular mechanisms involved in the suppression of bone formation, we have analyzed the effects of LPS on BSP gene expression. Bone sialoprotein (BSP) is a mineralized tissue-specific protein that appears to function in the initial mineralization of bone. Treatment of osteoblast-like ROS 17/2.8 cells with LPS (1 microg/ml) for 12 h caused a marked reduction in BSP mRNA levels. The addition of antioxidant N-acetylcysteine (NAC; 20 mM) 30 min prior to stimulation with LPS attenuated the inhibition of BSP mRNA levels. Transient transfection analyses, using chimeric constructs of the rat BSP gene promoter linked to a luciferase reporter gene, revealed that LPS (1 microg/ml) suppressed expression of luciferase construct, encompassing BSP promoter nucleotides -108 to +60, transfected into ROS17/2.8 cells. The effects of LPS were inhibited by protein kinase A (PKA) inhibitor, H89 and the tyrosine kinase inhibitor, herbimycin A (HA). Introduction of 2 bp mutations in the inverted CCAAT box (ATTGG; nts -50 and -46), a cAMP response element (CRE; nts -75 to -68), a FGF response element (FRE; nts -92 to -85), and a pituitary specific transcription factor binding element (Pit-1; nts -111 to -105) showed that the LPS effects were mediated by the CRE and FRE. Whereas the FRE and 3'-FRE DNA-protein complexes were decreased by LPS, CRE DNA-protein complex did not change after LPS treatment. These studies, therefore, show 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 BSP gene promoter.

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“…The soluble form of CD14 has also been investigated as a potential effector molecule in the interaction of the host and periodontopathogens. It has been reported that P. gingivalis LPS induces adhesion molecule expression in human gingival fibroblasts in a sCD14‐dependent manner (Masaka et al 1999). Soluble CD14 seems to mediate the response to LPS in cells lacking mCD14.…”

Section: Discussionmentioning

confidence: 99%

Flow‐cytometric analysis of lymphocyte subsets and mCD14 expression in patients with various periodontitis categories

Buduneli¹,

Bıçakçı²,

Keskinogˇlu³

2001

J Clinic Periodontology

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Soluble CD14‐Dependent Intercellular Adhesion Molecule‐1 Induction by Porphyromonas gingivalis Lipopolysaccharide in Human Gingival Fibroblasts

Abstract: These results indicate that P. gingivalis LPS induces ICAM-1 expression in HGF in an sCD14-dependent manner. The overexpression of ICAM-1 on fibroblasts in gingiva induced by P. gingivalis LPS seems to be involved in the retention of inflammatory cells in periodontitis lesions.

Cited by 11 publications

References 48 publications

CD14‐Mediated Induction of Interleukin‐8 and Monocyte Chemoattractant Protein‐1 by a Heat‐Resistant Constituent of Porphyromonas gingivalis in Endothelial Cells

CD14‐Mediated Induction of Interleukin‐8 and Monocyte Chemoattractant Protein‐1 by a Heat‐Resistant Constituent of Porphyromonas gingivalis in Endothelial Cells

Regulation of bone sialoprotein (BSP) gene transcription by lipopolysaccharide

Flow‐cytometric analysis of lymphocyte subsets and mCD14 expression in patients with various periodontitis categories

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