Lipid A‐associated proteins from <i>Porphyromonas gingivalis</i> stimulate release of nitric oxide by inducing expression of inducible nitric oxide synthase

Choi, Eun‐Young; Hwang, Yoon-Hwae; Lee, J.-Y.; Choi, Jae-Sung; Choi, Inhee; Jin, Ji-Young; Ko, Jea Seung; Kim, S.-J.

doi:10.1111/j.1600-0765.2006.00956.x

Cited by 10 publications

(12 citation statements)

References 49 publications

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“…However, the mechanisms by which these molecules mediate their pathogenic effects have not been fully delineated. Reports indicate that periodontopathic bacteria and bacterial components, including LPS, stimulate local gingival fibroblasts and inflammatory cells, including macrophages, to produce nitric oxide (2,7,12,17,41,46,61,66). In agreement with these findings, our data show for the first time that PDL cells also respond to an LPS challenge by producing increased levels of nitric oxide and iNOS.…”

Section: Discussionsupporting

confidence: 81%

“…Due to its small size and neutral charge, it can diffuse freely through the cell membrane and act as a signaling and effector molecule. iNOS is typically not present in a cell but can be induced when cells are stimulated by bacterial endotoxins and proinflammatory cytokines (12). Once induced, iNOS can produce nearmicromolar amounts of nitric oxide for sustained periods of time, and this production is independent of calcium ions.…”

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confidence: 99%

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Porphyromonas gingivalis, Gamma Interferon, and a Proapoptotic Fibronectin Matrix Form a Synergistic Trio That Induces c-Jun N-Terminal Kinase 1-Mediated Nitric Oxide Generation and Cell Death

Ghosh¹,

Park²,

Fenno

et al. 2008

Infect Immun

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During infection and inflammation, bacterial and inflammatory proteases break down extracellular matrices into macromolecular fragments. Fibronectin fragments are associated with disease severity in arthritis and periodontitis. The mechanisms by which these fragments contribute to disease pathogenesis are unclear. One likely mechanism is that fibronectin fragments induce apoptosis of resident cells, which can be further modulated by nitric oxide. Nitric oxide levels are increased at inflammatory sites in periodontitis patients. The aim of this study was to examine whether a proapoptotic fibronectin matrix (AFn) exerts its action by inducing nitric oxide and whether priming by bacterial and inflammatory components exacerbates this mechanism. Our data demonstrate that AFn increased the levels of nitric oxide and inducible nitric oxide synthase (iNOS) dose and time dependently in periodontal ligament (PDL) cells. These effects and apoptosis were inhibited by iNOS suppression and enhanced by iNOS overexpression. Nitric oxide and iNOS induction were paralleled by increased c-Jun N-terminal kinase 1 (JNK-1) phosphorylation. JNK-1 overexpression enhanced the expression of nitric oxide and iNOS, whereas inhibiting JNK-1 by small interfering RNA or a kinase mutant reversed these findings. Priming PDL cells with Porphyromonas gingivalis, its lipopolysaccharide (LPS), or gamma interferon (IFN-␥) further increased nitric oxide levels and apoptosis. Escherichia coli and Streptococcus mutans induced lesser effects. Gingival fibroblasts and neutrophils responded to a lesser degree to these stimuli, whereas keratinocytes were resistant to apoptosis. Thus, proapoptotic matrices trigger nitric oxide release via JNK-1, promoting further apoptosis in host cells. LPS and IFN-␥ accentuate this mechanism, suggesting that during inflammation, the affected matrices and bacterial and inflammatory components combined exert a greater pathogenic effect on host cells.

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Section: Discussionsupporting

confidence: 81%

mentioning

confidence: 99%

Porphyromonas gingivalis, Gamma Interferon, and a Proapoptotic Fibronectin Matrix Form a Synergistic Trio That Induces c-Jun N-Terminal Kinase 1-Mediated Nitric Oxide Generation and Cell Death

Ghosh¹,

Park²,

Fenno

et al. 2008

Infect Immun

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“…The cells were distributed to the plates at a concentration of 1×10 6 cells/mL and incubated for more than 2 h to attach the cells onto the plates. LPS (1 μg/mL) was treated with β-glucan and incubated for 24 h (Choi et al, 2007). …”

Section: Methodsmentioning

confidence: 99%

“…By using a 96 well plate, 100 μL of the Griess reagent (1% sulfanilamide, 0.1% naphthylethylene diamine dihydrochloride, and 2.5% phosphoric acid) (sigma), which was equivalent to the volume of the cell incubate supernatant, was mixed and reacted for 10 min to measure the absorbance at the wavelength of 540 nm using a Spectra Max 250 ELISA Reader (Molecular Devices, USA). The nitrite concentration was determined by using a standard curve that was produced by consecutively diluting NaNO 2 (sigma) with the incubate solution (Choi et al, 2007). …”

Section: Methodsmentioning

confidence: 99%

Effects of β-Glucan on the Release of Nitric Oxide by Macrophages Stimulated with Lipopolysaccharide

Choi

Lee

Hyeon

et al. 2016

Asian Australas. J. Anim. Sci

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This research analyzed the effect of β-glucan that is expected to alleviate the production of the inflammatory mediator in macrophagocytes, which are processed by the lipopolysaccharide (LPS) of Escherichia. The incubated layer was used for a nitric oxide (NO) analysis. The DNA-binding activation of the small unit of nuclear factor-κB was measured using the enzyme-linked immunosorbent assay-based kit. In the RAW264.7 cells that were vitalized by Escherichia coli (E. coli) LPS, the β-glucan inhibited both the combatant and rendering phases of the inducible NO synthase (iNOS)-derived NO. β-Glucan increased the expression of the heme oxygenase-1 (HO-1) in the cells that were stimulated by E. coli LPS, and the HO-1 activation was inhibited by the tin protoporphyrin IX (SnPP). This shows that the NO production induced by LPS is related to the inhibition effect of β-glucan. The phosphorylation of c-Jun N-terminal kinases (JNK) and the p38 induced by the LPS were not influenced by the β-glucan, and the inhibitory κB-α (IκB-α) decomposition was not influenced either. Instead, β-glucan remarkably inhibited the phosphorylation of the signal transducer and activator of transcription-1 (STAT1) that was induced by the E. coli LPS. Overall, the β-glucan inhibited the production of NO in macrophagocytes that was vitalized by the E .coli LPS through the HO-1 induction and the STAT1 pathways inhibition in this research. As the host immune response control by β-glucan weakens the progress of the inflammatory disease, β-glucan can be used as an effective immunomodulator.

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“…The detection of high amounts of the NO precursors L-arginine and L-citrullin in inflamed gingival tissue in vivo (Matejka et al 1998), and iNOS expression in macrophages, lymphocytes and PMN neutrophils in experimentallyinduced periodontitis in rat (Lohinai et al 1998) as well as in macrophages, endothelial cells (Lappin et al 2000) and PMNs (Batista et al 2002) in human periodontitis suggests the production and participation of NO in PD. Attempting to throw light on the signaling mechanisms involved in induced NO production by a murine macrophage cell line, the study of Choi et al (2007) indicated that multiple signaling pathways, such as nuclear factor-jB, protein tyrosine kinase, protein kinase C, and MAPK cascades, are coordinated in NO production induced by P. gingivalis lipid A-associated protein.…”

Section: Introductionmentioning

confidence: 99%

Morphologic evaluation and expression of matrix metalloproteinases-2 and 9 and nitric oxide during experimental periodontal disease in rat

et al. 2008

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The immunopathologic and inflammatory mechanisms involved in periodontal disease (PD) include the participation of host resident, inflammatory cells and chemical mediators. Metalloproteinases (MMPs) and nitric oxide (NO) play essential role in extracellular matrix turnover of periodontal tissue destruction. In this study, by means of RT-PCR through semi-quantitative densitometric scanning methods, the expression of MMPs -2 and -9 and inducible NO synthase (iNOS) was temporally and spatially investigated during the destructive mechanisms of experimentally induced PD in rats. Samples from different periods were microscopically analyzed and compared with the contralateral side (control). Our results showed significant expression of MMP-9 and iNOS in tissues affected by PD, as compared with controls, three days after PD induction, simultaneously with the beginning of alveolar bone loss. At 7 days post induction, only the MMP-9 mRNA presented a significantly higher expression, as compared with the respective controls. Thus, in the rat ligature-induced PD, MMP-9 and iNOS might importantly participate in the early stages of the disease, including inflammatory cell migration, tissue destruction and alveolar bone resorption. Also, we may suggest that the exuberant presence of PMNs may be related to the important expression of iNOS and MMP-9 found at 3 days post induction.

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Lipid A‐associated proteins from Porphyromonas gingivalis stimulate release of nitric oxide by inducing expression of inducible nitric oxide synthase

Cited by 10 publications

References 49 publications

Porphyromonas gingivalis, Gamma Interferon, and a Proapoptotic Fibronectin Matrix Form a Synergistic Trio That Induces c-Jun N-Terminal Kinase 1-Mediated Nitric Oxide Generation and Cell Death

Porphyromonas gingivalis, Gamma Interferon, and a Proapoptotic Fibronectin Matrix Form a Synergistic Trio That Induces c-Jun N-Terminal Kinase 1-Mediated Nitric Oxide Generation and Cell Death

Effects of β-Glucan on the Release of Nitric Oxide by Macrophages Stimulated with Lipopolysaccharide

Morphologic evaluation and expression of matrix metalloproteinases-2 and 9 and nitric oxide during experimental periodontal disease in rat

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