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Critical Reviews in Oral Biology & Medicine
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PORPHYROMONAS GINGIVALIS LIPOPOLYSACCHARIDE SIGNALING IN GINGIVAL FIBROBLASTS–CD14 AND TOLL-LIKE RECEPTORS

P.-L. Wang* and K. Ohura

Department of Pharmacology, Osaka Dental University, 8-1 Kuzuhahanazono-cho, Hirakata, Osaka 573-1121, Japan;


Figure 1
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  		Figure 1. Endotoxins reside in the outer membrane of Gram-negative bacteria. The cut reveals the structure of the two membranes that envelop the bacterium (Rietschel and Brade, 1992).

 

Figure 2
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  		Figure 2. Effects of anti-CD14 monoclonal antibody (A) and anti-Toll-like receptor 4 monoclonal antibody (B) on the binding of FITC-labeled LPS to human gingival fibroblasts. Human gingival fibroblasts were incubated with an unlabeled control antibody (CT), FITC-labeled LPS (LPS binding), or anti-CD14 monoclonal antibody with FITC-labeled LPS (LPS+anti-CD14 mAb) and anti-Toll-like receptor 4 monoclonal antibody with FITC-labeled LPS (LPS+anti-TLR4 mAb). The cells were analyzed by flow cytometry (Wang et al., 1998, 2000b).

 

Figure 3
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  		Figure 3. Analysis of protein phosphorylation by Western blot analysis. Human gingival fibroblasts were stimulated with LPS from Porphyromonas gingivalis (P-LPS) in the presence or absence of anti-CD14 monoclonal antibody (anti-CD14 mAb). (A) The cells were subjected to Western blotting with anti-phosphotyrosine monoclonal antibody. (B) The immunoprecipitate was analyzed with anti-mitogen-activated protein kinase (MAPK: ERK2 and ERK1) kinase monoclonal antibody (Wang et al., 1996, 1998). The lanes are as follows: non-stimulated cells (lane 1), LPS-stimulated (lane 2), anti-CD14 mAb (lane 3), and both LPS and anti-CD14 mAb (lane 4).

 

Figure 4
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  		Figure 4. Analysis of protein phosphorylation by Western blot analysis. Human gingival fibroblasts were stimulated with LPS from Porphyromonas gingivalis (P-LPS) in the presence or absence of anti-Toll-like receptor 4 (TLR4) monoclonal antibody (anti-TLR4 mAb). (A) The cells were subjected to Western blotting with anti-phosphotyrosine monoclonal antibody. (B) The immunoprecipitate was analyzed with anti-IL-1 receptor-associated kinase (IRAK) monoclonal antibody (Wang et al., 2000a,b).

 

Figure 5
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  		Figure 5. Porphyromonas gingivalis LPS induces NF-{kappa}B and AP-1 expression in human gingival fibroblasts. The cells were stimulated with LPS from Porphyromonas gingivalis (P-LPS) in the presence or absence of anti-TLR4 monoclonal antibody (anti-TLR4 mAb). Gel mobility shift assay was performed with a biotin-labeled probe [NF-{kappa}B (A) or AP-1 (B)] (Wang et al., 2000a,b).

 

Figure 6
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  		Figure 6. A hypothetical model of Porphyromonas gingivalis LPS signaling via CD14 and TLR4 in gingival fibroblasts. The diagram shows the signaling cascade from the binding of the signaling complex to CD14 or TLR4 to the activation of NF-{kappa}B and AP-1. P.g. LPS, Porphyromonas gingivalis lipopolysaccharide; TLR4, Toll-like receptor 4; MyD88, myeloid differentiation primary response gene 88; IRAK, IL-1 receptor accessory protein kinase; TRAF6, TNF receptor-associated factor; TAK1, transforming growth factor-β-activated kinase1; TAB1, TAK1 binding protein1; MAPKK, map kinase kinase; AP-1, activating protein-1; JNK/p38, Jun N-terminal kinase/p38; NIK, NF-{kappa}B-inducing kinase; IKK, inhibitor of nuclear factor-{kappa}B; NF-{kappa}B, nuclear factor-{kappa}B.

 

Critical Reviews in Oral Biology & Medicine, Vol. 13, No. 2, 132-142 (2002)
DOI: 10.1177/154411130201300204
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