Log in

Relevant bibliographies by topics / Porphyromonas gingivalis lipopolysaccharide / Journal articles

Journal articles on the topic 'Porphyromonas gingivalis lipopolysaccharide'

To see the other types of publications on this topic, follow the link: Porphyromonas gingivalis lipopolysaccharide.

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Porphyromonas gingivalis lipopolysaccharide.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Jain, Sumita, and Richard P. Darveau. "Contribution of Porphyromonas gingivalis lipopolysaccharide to periodontitis." Periodontology 2000 54, no. 1 (August 16, 2010): 53–70. http://dx.doi.org/10.1111/j.1600-0757.2009.00333.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Al-Qutub, Montaser N., Pamela H. Braham, Lisa M. Karimi-Naser, Xinyan Liu, Caroline A. Genco, and Richard P. Darveau. "Hemin-Dependent Modulation of the Lipid A Structure of Porphyromonas gingivalis Lipopolysaccharide." Infection and Immunity 74, no. 8 (August 2006): 4474–85. http://dx.doi.org/10.1128/iai.01924-05.

Full text

Abstract:

ABSTRACT Porphyromonas gingivalis is a periopathogen strongly associated with the development of adult-type periodontitis. Both the virulence characteristics of periopathogens and host-related factors are believed to contribute to periodontitis. P. gingivalis lipopolysaccharide (LPS) displays a significant amount of lipid A structural heterogeneity, containing both penta- and tetra-acylated lipid A structures. However, little is known concerning how the lipid A structural content of P. gingivalis is regulated. Alterations in the lipid A content may facilitate the ability of P. gingivalis to modulate the innate host response to this bacterium. In this report, it is shown that the concentration of hemin in the growth medium significantly modulates the lipopolysaccharide lipid A structural content of P. gingivalis. Hemin is a key microenvironmental component of gingival cervicular fluid which is believed to vary depending upon the state of vascular ulceration. At low hemin concentrations, one major penta-acylated lipid A structure was found, whereas at high concentrations of hemin, multiple tetra- and penta-acylated lipid A structures were observed. Hemin concentrations, not iron acquisition, were responsible for the alterations in the lipid A structural content. The modifications of the lipid A structural content were independent of the LPS extraction procedure and occurred in a variety of laboratory strains as well as a freshly obtained clinical isolate. The known hemin binding proteins Kgp and HmuR contributed to the lipid A modulation sensing mechanism. To the best of our knowledge, this is the first report that hemin, a clinically relevant microenvironmental component for P. gingivalis, can modulate the lipid A structure found in a bacterium. Since tetra- and penta-acylated P. gingivalis lipid A structures have opposing effects on Toll-like receptor 4 activation, the alteration of the lipid A structural content may have significant effects on the host response to this bacterium.

APA, Harvard, Vancouver, ISO, and other styles

3

Han, Su-Ji, So-Yeon Jeong, Yun-Ju Nam, Kyu-Ho Yang, Hoi-Soon Lim, and Jin Chung. "Xylitol Inhibits Inflammatory Cytokine Expression Induced by Lipopolysaccharide from Porphyromonas gingivalis." Clinical Diagnostic Laboratory Immunology 12, no. 11 (November 2005): 1285–91. http://dx.doi.org/10.1128/cdli.12.11.1285-1291.2005.

Full text

Abstract:

ABSTRACT Porphyromonas gingivalis is one of the suspected periodontopathic bacteria. The lipopolysaccharide (LPS) of P. gingivalis is a key factor in the development of periodontitis. Inflammatory cytokines play important roles in the gingival tissue destruction that is a characteristic of periodontitis. Macrophages are prominent at chronic inflammatory sites and are considered to contribute to the pathogenesis of periodontitis. Xylitol stands out and is widely believed to possess anticaries properties. However, to date, little is known about the effect of xylitol on periodontitis. The aim of the present study was to determine tumor necrosis factor alpha (TNF-α) and interleukin-1β (IL-1β) expression when RAW 264.7 cells were stimulated with P. gingivalis LPS (hereafter, LPS refers to P. gingivalis LPS unless stated otherwise) and the effect of xylitol on the LPS-induced TNF-α and IL-1β expression. The kinetics of TNF-α and IL-1β levels in culture supernatant after LPS treatment showed peak values at 1 h (TNF-α) and 2 to 4 h (IL-1β), respectively. NF-κB, a transcription factor, was also activated by LPS treatment. These cytokine expressions and NF-κB activation were suppressed by pretreatment with pyrrolidine dithiocarbamate (an inhibitor of NF-κB). Pretreatment with xylitol inhibited LPS-induced TNF-α and IL-1β gene expression and protein synthesis. LPS-induced mobilization of NF-κB was also inhibited by pretreatment with xylitol in a dose-dependent manner. Xylitol also showed inhibitory effect on the growth of P. gingivalis. Taken together, these findings suggest that xylitol may have good clinical effect not only for caries but also for periodontitis by its inhibitory effect on the LPS-induced inflammatory cytokine expression.

APA, Harvard, Vancouver, ISO, and other styles

4

Tada, Hiroyuki, Shunji Sugawara, Eiji Nemoto, Nobuhiro Takahashi, Takahisa Imamura, Jan Potempa, James Travis, Hidetoshi Shimauchi, and Haruhiko Takada. "Proteolysis of CD14 on Human Gingival Fibroblasts by Arginine-Specific Cysteine Proteinases from Porphyromonas gingivalis Leading to Down-Regulation of Lipopolysaccharide-Induced Interleukin-8 Production." Infection and Immunity 70, no. 6 (June 2002): 3304–7. http://dx.doi.org/10.1128/iai.70.6.3304-3307.2002.

Full text

Abstract:

ABSTRACT Arginine-specific cysteine proteinases (gingipains-R) from periodontopathic Porphyromonas gingivalis cleaved CD14, a bacterial pattern recognition receptor, on human gingival fibroblasts (HGF). Consequently, gingipains-R reduced lipopolysaccharide-induced interleukin-8 production by HGF, indicating that gingipains-R inhibited CD14-dependent HGF activation and are involved in immune evasion by the bacterium in periodontal tissues.

APA, Harvard, Vancouver, ISO, and other styles

5

Knoernschild, Kent L., Geoffrey R. Tompkins, Carol A. Lefebvre, and George S. Schuster. "Porphyromonas gingivalis lipopolysaccharide affinity for two casting alloys." Journal of Prosthetic Dentistry 74, no. 1 (July 1995): 33–38. http://dx.doi.org/10.1016/s0022-3913(05)80225-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Ferraz, Caio Cezar Randi, Michael A. Henry, Kenneth M. Hargreaves, and Anibal Diogenes. "Lipopolysaccharide From Porphyromonas gingivalis Sensitizes Capsaicin-Sensitive Nociceptors." Journal of Endodontics 37, no. 1 (January 2011): 45–48. http://dx.doi.org/10.1016/j.joen.2007.07.001.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Khan, Junad, Bollama Puchimada, Daniel Kadouri, Tali Zusman, Fawad Javed, and Eli Eliav. "The anti-nociceptive effects of Porphyromonas gingivalis lipopolysaccharide." Archives of Oral Biology 102 (June 2019): 193–98. http://dx.doi.org/10.1016/j.archoralbio.2019.04.012.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Bozkurt, S. Buket, Sema S. Hakki, Erdogan E. Hakki, Yusuf Durak, and Alpdogan Kantarci. "Porphyromonas gingivalis Lipopolysaccharide Induces a Pro-inflammatory Human Gingival Fibroblast Phenotype." Inflammation 40, no. 1 (November 3, 2016): 144–53. http://dx.doi.org/10.1007/s10753-016-0463-7.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Rangarajan, Minnie, Joseph Aduse-Opoku, Nikolay Paramonov, Ahmed Hashim, Nagihan Bostanci, Owen P. Fraser, Edward Tarelli, and Michael A. Curtis. "Identification of a Second Lipopolysaccharide in Porphyromonas gingivalis W50." Journal of Bacteriology 190, no. 8 (February 8, 2008): 2920–32. http://dx.doi.org/10.1128/jb.01868-07.

Full text

Abstract:

ABSTRACT We previously described a cell surface anionic polysaccharide (APS) in Porphyromonas gingivalis that is required for cell integrity and serum resistance. APS is a phosphorylated branched mannan that shares a common epitope with posttranslational additions to some of the Arg-gingipains. This study aimed to determine the mechanism of anchoring of APS to the surface of P. gingivalis. APS was purified on concanavalin A affinity columns to minimize the loss of the anchoring system that occurred during chemical extraction. 1H nuclear magnetic resonance spectroscopy of the lectin-purified APS confirmed the previous structure but also revealed additional signals that suggested the presence of a lipid A. This was confirmed by fatty acid analysis of the APS and matrix-assisted laser desorption ionization-time of flight mass spectrometry of the lipid A released by treatment with sodium acetate buffer (pH 4.5). Hence, P. gingivalis synthesizes two distinct lipopolysaccharide (LPS) macromolecules containing different glycan repeating units: O-LPS (with O-antigen tetrasaccharide repeating units) and A-LPS (with APS repeating units). Nonphosphorylated penta-acylated and nonphosphorylated tetra-acylated species were detected in lipid A from P. gingivalis total LPS and in lipid A from A-LPS. These lipid A species were unique to lipid A derived from A-LPS. Biological assays demonstrated a reduced proinflammatory activity of A-LPS compared to that of total LPS. Inactivation of a putative O-antigen ligase (waaL) at PG1051, which is required for the final step of LPS biosynthesis, abolished the linkage of both the O antigen and APS to the lipid A core of O-LPS and A-LPS, respectively, suggesting that WaaL in P. gingivalis has dual specificity for both O-antigen and APS repeating units.

APA, Harvard, Vancouver, ISO, and other styles

10

Bachtiar, Endang Winiati, Citra F. Putri, Retno D. Soejoedono, and Boy M. Bachtiar. "Expression of TNF, IL1B, and NOS2 in the neural cell after induced by Porphyromonas gingivalis with and without coating antibody anti-Porphyromonas gingivalis." F1000Research 9 (March 17, 2021): 1499. http://dx.doi.org/10.12688/f1000research.26749.2.

Full text

Abstract:

Porphyromonas gingivalis has virulence factors such as gingipain and lipopolysaccharide, causing bacteremia to reach the brain and activate neuroinflammatory release cytokines. This study analyzed the effect of the co-culture of neuron cells with P. gingivalis coated with anti-P. gingivalis antibodies against cytokines produced by neuron cells. The gene expressions of the TNF, IL1B, NOS2 in neurons was evaluated using RT-qPCR. The results showed that P. gingivalis coated with anti-P. gingivalis antibody before co-culture with neuron cells could decrease the gene expression of TNF, IL1B, and NOS2 of neuron cells.

APA, Harvard, Vancouver, ISO, and other styles

11

Bachtiar, Endang Winiati, Citra F. Putri, Retno D. Soejoedono, and Boy M. Bachtiar. "Expression of TNF, IL1B, and iNOS2 in the neural cell after induced by Porphyromonas gingivalis with and without coating antibody anti-Porphyromonas gingivalis." F1000Research 9 (April 28, 2021): 1499. http://dx.doi.org/10.12688/f1000research.26749.3.

Full text

Abstract:

Porphyromonas gingivalis has virulence factors such as gingipain and lipopolysaccharide, causing bacteremia to reach the brain and activate neuroinflammatory release cytokines. This study analyzed the effect of the co-culture of neuron cells with P. gingivalis coated with anti-P. gingivalis antibodies against cytokines produced by neuron cells. The gene expressions of the TNF, IL1B, iNOS2 in neurons was evaluated using RT-qPCR. The results showed that P. gingivalis coated with anti-P. gingivalis antibody before co-culture with neuron cells could decrease the gene expression of TNF, IL1B, and iNOS2 of neuron cells.

APA, Harvard, Vancouver, ISO, and other styles

12

Bachtiar, Endang Winiati, Citra F. Putri, Retno D. Soejoedono, and Boy M. Bachtiar. "Expression of TNF, IL1B, and iNOS2 in the neural cell after induced by Porphyromonas gingivalis with and without coating antibody anti-Porphyromonas gingivalis." F1000Research 9 (June 28, 2021): 1499. http://dx.doi.org/10.12688/f1000research.26749.4.

Full text

Abstract:

Porphyromonas gingivalis has virulence factors such as gingipain and lipopolysaccharide, causing bacteremia to reach the brain and activate neuroinflammatory release cytokines. This study analyzed the effect of the co-culture of neuron cells with P. gingivalis coated with anti-P. gingivalis antibodies against cytokines produced by neuron cells. The gene expressions of the TNF, IL1B, iNOS2 in neurons was evaluated using RT-qPCR. The results showed that P. gingivalis coated with anti-P. gingivalis antibody before co-culture with neuron cells could decrease the gene expression of TNF, IL1B, and iNOS2 of neuron cells.

APA, Harvard, Vancouver, ISO, and other styles

13

Bachtiar, Endang Winiati, Citra F. Putri, Retno D. Soejoedono, and Boy Muchlis Bachtiar. "Expression of TNF, IL1B, and NOS2 in the neural cell after induced by Porphyromonas gingivalis with and without coating antibody anti-Porphyromonas gingivalis." F1000Research 9 (December 23, 2020): 1499. http://dx.doi.org/10.12688/f1000research.26749.1.

Full text

Abstract:

Porphyromonas gingivalis has virulence factors such as gingipain and lipopolysaccharide, causing bacteremia to reach the brain and activate neuroinflammatory release cytokines. This study analyzed the effect of the co-culture of neuron cells with P. gingivalis coated with anti-P. gingivalis antibodies against cytokines produced by neuron cells. The gene expressions of the TNF, IL1B, NOS2 in neurons was evaluated using RT-qPCR. The results showed that P. gingivalis coated with anti-P. gingivalis antibody before co-culture with neuron cells could decrease the gene expression of TNF, IL1B, and NOS2 of neuron cells.

APA, Harvard, Vancouver, ISO, and other styles

14

Murray, D. A., and J. M. A. Wilton. "Lipopolysaccharidefrom the Periodontal Pathogen Porphyromonas gingivalisPrevents Apoptosis of HL60-Derived Neutrophils InVitro." Infection and Immunity 71, no. 12 (December 2003): 7232–35. http://dx.doi.org/10.1128/iai.71.12.7232-7235.2003.

Full text

Abstract:

ABSTRACT Lipopolysaccharide (LPS) from Porphyromonas gingivalis prevented apoptosis of HL60-derived neutrophils, which could not be restored upon the addition of interleukin-10. Signaling of P. gingivalis LPS through Toll-like receptor 2 (TLR2), not TLR4, may account for the inhibiting effect of P. gingivalis LPS on apoptosis and provide a mechanism for the development of destructive periodontal inflammation.

APA, Harvard, Vancouver, ISO, and other styles

15

Memedovski, Zylfi, Evan Czerwonka, Jin Han, Joshua Mayer, Margaret Luce, Lucas C. Klemm, Mary L. Hall, and Alejandro M. S. Mayer. "Classical and Alternative Activation of Rat Microglia Treated with Ultrapure Porphyromonas gingivalis Lipopolysaccharide In Vitro." Toxins 12, no. 5 (May 19, 2020): 333. http://dx.doi.org/10.3390/toxins12050333.

Full text

Abstract:

The possible relationship between periodontal disease resulting from the infection of gingival tissue by the Gram-negative bacterium Porphyromonas gingivalis (P. gingivalis) and the development of neuroinflammation remains under investigation. Recently, P. gingivalis lipopolysaccharide (LPS) was reported in the human brain, thus suggesting it might activate brain microglia, a cell type participating in neuroinflammation. We tested the hypothesis of whether in vitro exposure to ultrapure P. gingivalis LPS may result in classical and alternative activation phenotypes of rat microglia, with the concomitant release of cytokines and chemokines, as well as superoxide anion (O2−), thromboxane B2 (TXB2), and matrix metalloprotease-9 (MMP-9). After an 18-h exposure of microglia to P. gingivalis LPS, the concentration-dependent responses were the following: 0.1–100 ng/mL P. gingivalis LPS increased O2− generation, with reduced inflammatory mediator generation; 1000–10,000 ng/mL P. gingivalis LPS generated MMP-9, macrophage inflammatory protein 1α (MIP-1α/CCL3), macrophage inflammatory protein-2 (MIP-2/CXCL2) release and significant O2− generation; 100,000 ng/mL P. gingivalis LPS sustained O2− production, maintained MMP-9, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) release, and triggered elevated levels of MIP-1α/CCL3, MIP-2/CXCL2, and cytokine-induced neutrophil chemoattractant 1 (CINC-1/CXCL-1), with a very low release of lactic dehydrogenase (LDH). Although P. gingivalis LPS was less potent than Escherichia coli (E. coli) LPS in stimulating TXB2, MMP-9, IL-6 and interleukin 10 (IL-10) generation, we observed that it appeared more efficacious in enhancing the release of O2−, TNF-α, MIP-1α/CCL3, MIP-2/CXCL2 and CINC-1/CXCL-1. Our results provide support to our research hypothesis because an 18-h in vitro stimulation with ultrapure P. gingivalis LPS resulted in the classical and alternative activation of rat brain microglia and the concomitant release of cytokines and chemokines.

APA, Harvard, Vancouver, ISO, and other styles

16

Coats, Stephen R., Robert A. Reife, Brian W. Bainbridge, Thu-Thao T. Pham, and Richard P. Darveau. "Porphyromonasgingivalis Lipopolysaccharide Antagonizes Escherichiacoli Lipopolysaccharide at Toll-Like Receptor 4 in HumanEndothelialCells." Infection and Immunity 71, no. 12 (December 2003): 6799–807. http://dx.doi.org/10.1128/iai.71.12.6799-6807.2003.

Full text

Abstract:

ABSTRACT E. coli lipopolysaccharide (LPS) induces cytokine and adhesion molecule expression via the toll-like receptor 4 (TLR4) signaling complex in human endothelial cells. In the present study, we investigated the mechanism by which Porphyromonas gingivalis LPS antagonizes E. coli LPS-dependent activation of human endothelial cells. P. gingivalis LPS at 1 μg/ml inhibited both E. coli LPS (10 ng/ml) and Mycobacterium tuberculosis heat shock protein (HSP) 60.1 (10 μg/ml) stimulation of E-selectin mRNA expression in human umbilical vein endothelial cells (HUVEC) without inhibiting interleukin-1 beta (IL-1β) stimulation. P. gingivalis LPS (1μ g/ml) also blocked both E. coli LPS-dependent and M. tuberculosis HSP60.1-dependent but not IL-1β-dependent activation of NF-κB in human microvascular endothelial (HMEC-1) cells, consistent with antagonism occurring upstream from the TLR/IL-1 receptor adaptor protein, MyD88. Surprisingly, P. gingivalis LPS weakly but significantly activated NF-κB in HMEC-1 cells in the absence of E. coli LPS, and the P. gingivalis LPS-dependent agonism was blocked by transient expression of a dominant negative murine TLR4. Pretreatment of HUVECs with P. gingivalis LPS did not influence the ability of E. coli LPS to stimulate E-selectin mRNA expression. Taken together, these data provide the first evidence that P. gingivalis LPS-dependent antagonism of E. coli LPS in human endothelial cells likely involves the ability of P. gingivalis LPS to directly compete with E. coli LPS at the TLR4 signaling complex.

APA, Harvard, Vancouver, ISO, and other styles

17

Swietnicki, Wieslaw, and Ron Caspi. "Prediction of Selected Biosynthetic Pathways for the Lipopolysaccharide Components in Porphyromonas gingivalis." Pathogens 10, no. 3 (March 20, 2021): 374. http://dx.doi.org/10.3390/pathogens10030374.

Full text

Abstract:

Porphyromonas gingivalis is an oral human pathogen. The bacterium destroys dental tissue and is a serious health problem worldwide. Experimental data and bioinformatic analysis revealed that the pathogen produces three types of lipopolysaccharides (LPS): normal (O-type), anionic (A-type), and capsular (K-type). The enzymes involved in the production of all three types of lipopolysaccharide have been largely identified for the first two and partially for the third type. In the current work, we use bioinformatics tools to predict biosynthetic pathways for the production of the normal (O-type) lipopolysaccharide in the W50 strain Porphyromonas gingivalis and compare the pathway with other putative pathways in fully sequenced and completed genomes of other pathogenic strains. Selected enzymes from the pathway have been modeled and putative structures are presented. The pathway for the A-type antigen could not be predicted at this time due to two mutually exclusive structures proposed in the literature. The pathway for K-type antigen biosynthesis could not be predicted either due to the lack of structural data for the antigen. However, pathways for the synthesis of lipid A, its core components, and the O-type antigen ligase reaction have been proposed based on a combination of experimental data and bioinformatic analyses. The predicted pathways are compared with known pathways in other systems and discussed. It is the first report in the literature showing, in detail, predicted pathways for the synthesis of selected LPS components for the model W50 strain of P. gingivalis.

APA, Harvard, Vancouver, ISO, and other styles

18

Tamai, Riyoko, Michiyo Kobayashi-Sakamoto, and Yusuke Kiyoura. "Extracellular galectin-1 enhances adhesion to and invasion of oral epithelial cells by Porphyromonas gingivalis." Canadian Journal of Microbiology 64, no. 7 (July 2018): 465–71. http://dx.doi.org/10.1139/cjm-2017-0461.

Full text

Abstract:

Galectin-1 and galectin-3 are C-type lectin receptors that bind to lipopolysaccharide in the cell wall of gram-negative bacteria. In this study, we investigated the effects of galectin-1 and galectin-3 on adhesion to and invasion of the human gingival epithelial cell line Ca9-22 by Porphyromonas gingivalis, a periodontal pathogenic gram-negative bacterium. Recombinant galectin-1, but not galectin-3, enhanced P. gingivalis adhesion and invasion, although both galectins bound similarly to P. gingivalis. Flow cytometry also revealed that Ca9-22 cells express low levels of galectin-1 and moderate levels of galectin-3. Ca9-22 cells in which galectin-3 was knocked-down did not exhibit enhanced P. gingivalis adhesion and invasion. Similarly, specific antibodies to galectin-1 and galectin-3 did not inhibit P. gingivalis adhesion and invasion. These results suggest that soluble galectin-1, but not galectin-3, may exacerbate periodontal disease by enhancing the adhesion to and invasion of host cells by periodontal pathogenic bacteria.

APA, Harvard, Vancouver, ISO, and other styles

19

Zhou, Qingde, Tesfahun Desta, Matthew Fenton, Dana T. Graves, and Salomon Amar. "Cytokine Profiling of Macrophages Exposed to Porphyromonas gingivalis, Its Lipopolysaccharide, or Its FimA Protein." Infection and Immunity 73, no. 2 (February 2005): 935–43. http://dx.doi.org/10.1128/iai.73.2.935-943.2005.

Full text

Abstract:

ABSTRACT To characterize the roles of Porphyromonas gingivalis and its components in the disease processes, we investigated the cytokine profile induced by live P. gingivalis, its lipopolysaccharides (LPS), and its major fimbrial protein, fimbrillin (FimA). Using cytokine antibody arrays, we found that P. gingivalis LPS and FimA induced a similar profile of cytokine expression when exposed to mouse peritoneal macrophages but that this profile differed significantly in response to live P. gingivalis. In vitro, mouse peritoneal macrophages were stimulated to produce interleukin-6 (IL-6), granulocyte colony-stimulating factor, and lymphotactin by live P. gingivalis, but not by P. gingivalis LPS or FimA, while RANTES, gamma interferon, IL-17, vascular cell adhesion molecule 1 (VCAM-1), and vascular endothelial growth factor were induced by P. gingivalis LPS or FimA, but not by live P. gingivalis. In vivo, IL-6 mRNA was strongly induced only by live P. gingivalis while monocyte chemoattractant protein 1 mRNA was strongly induced only by P. gingivalis LPS and FimA in mouse calvarial scalp, further confirming the differences of cytokine profile induced in vitro. Cytokine antibody arrays using toll-like receptor 2 (TLR2)- and TLR4-deficient macrophages revealed that most of the cytokines induced by P. gingivalis LPS or FimA signal through TLR2, while most of cytokines induced by live P. gingivalis signal through both TLR2 and TLR4. Interestingly, the activation of TLR2 by live P. gingivalis inhibited the release of RANTES, VCAM-1, and IL-1α from mouse peritoneal macrophages. A tumor necrosis factor alpha enzyme-linked immunosorbent assay further confirmed that P. gingivalis LPS and FimA activate mouse peritoneal macrophages via TLR2. These results indicate that host immune cells sense live P. gingivalis and its components differently, which translates into the expression of different inflammatory cytokine profiles.

APA, Harvard, Vancouver, ISO, and other styles

20

Watanabe, A., A. Takeshita, S. Kitano, and S. Hanazawa. "CD14-mediated signal pathway of Porphyromonas gingivalis lipopolysaccharide in human gingival fibroblasts." Infection and immunity 64, no. 11 (1996): 4488–94. http://dx.doi.org/10.1128/iai.64.11.4488-4494.1996.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Li, Yuyang, Baosheng Li, Yujie Liu, Haoyang Wang, Mengxiao He, Yanqun Liu, Yidan Sun, and Weiyan Meng. "Porphyromonas gingivalis lipopolysaccharide affects oral epithelial connections via pyroptosis." Journal of Dental Sciences 16, no. 4 (October 2021): 1255–63. http://dx.doi.org/10.1016/j.jds.2021.01.003.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Teraoka, Yuko, Haruhisa Konishi, Satoshi Urabe, Jun Sugimoto, and Yoshiki Kudo. "Porphyromonas gingivalis-lipopolysaccharide enhances inflammation in amniotic mesenchymal cells." Placenta 103 (January 2021): 251–52. http://dx.doi.org/10.1016/j.placenta.2020.09.034.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

ISOGAI, Emiko, Hiroshi ISOGAI, Kimiharu HIROSE, Hiroko MIMURA, Koichi KIMURA, Shunji HAYASHI, Masanobu HAYASHI, Nobuhiro FUJII, and Yoshimi BENNO. "Platelet Responses after Stimulation with Lipopolysaccharide from Porphyromonas gingivalis." Bioscience and Microflora 16, no. 2 (1997): 79–82. http://dx.doi.org/10.12938/bifidus1996.16.79.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Veloso, Pablo, Alejandra Fernández, Jessica Astorga, David González-Quintanilla, Alfredo Castro, Alejandro Escobar, Anilei Hoare, and Marcela Hernández. "Lipopolysaccharide from Porphyromonas gingivalis, but Not from Porphyromonas endodontalis, Induces Macrophage M1 Profile." International Journal of Molecular Sciences 23, no. 17 (September 2, 2022): 10011. http://dx.doi.org/10.3390/ijms231710011.

Full text

Abstract:

Apical Lesions of Endodontic Origin (ALEO) are initiated by polymicrobial endodontic canal infection. Porphyromonas gingivalis (Pg) and Porphyromonas endodontalis (Pe) lipopolysaccharides (LPS) can induce a pro-inflammatory macrophage response through their recognition by TLR2 and TLR4. However, polarization responses induced by Pg and/or Pe LPS in macrophages are not fully understood. We aimed to characterize the polarization profiles of macrophages differentiated from THP-1 cells following Pg and/or Pe LPS stimulation from reference strain and clinical isolates. A modified LPS purification protocol was implemented and the electrophoretic LPS profiles were characterized. THP-1 human monocytes differentiated to macrophages were stimulated with Pg and Pe LPS. Polarization profiles were characterized through cell surface markers and secreted cytokines levels after 24 h of stimulation. TLR2 and TLR4 cell surfaces and transcriptional levels were determined after 24 or 2 h of LPS stimulation, respectively. LPS from Pg induced a predominant M1 profile in macrophages evidenced by changes in the expression of the surface marker CD64 and pro-inflammatory cytokine profiles, TNF-α, IL-1β, IL-6, and IL-12. Pe LPS was unable to induce a significant response. TLR2 and TLR4 expressions were neither modified by Pg or Pe LPS. Pg LPS, but not Pe LPS, induced a macrophage M1 Profile.

APA, Harvard, Vancouver, ISO, and other styles

25

Olsen, Ingar, Douglas B. Kell, and Etheresia Pretorius. "Is Porphyromonas gingivalis involved in Parkinson’s disease?" European Journal of Clinical Microbiology & Infectious Diseases 39, no. 11 (June 21, 2020): 2013–18. http://dx.doi.org/10.1007/s10096-020-03944-2.

Full text

Abstract:

Abstract Porphyromonas gingivalis, a major subgingival plaque bacterium in periodontitis, has recently attracted much attention as a possible microbial driver in Alzheimer’s disease. In the present paper, another common neuroinflammatory disease, Parkinson’s disease (PD), is discussed. A recent study found major virulence factors of P. gingivalis such as gingipain R1 (RgpA) and lipopolysaccharide in the blood circulation of a PD population. The current review reveals how features such as systemic inflammation, hypercoagulation, presence of amyloid fibrin(ogen) in plasma, and marked ultrastructural changes in platelets, probably induced by P. gingivalis, may affect the development of PD. Several other clinical studies have also demonstrated an association between periodontitis and PD. Even if the risk of periodontal diseases causing neurological disorders needs to be better substantiated, that should not keep us from trying to prevent them by performing careful daily dental hygiene.

APA, Harvard, Vancouver, ISO, and other styles

26

Kocgozlu, L., R. Elkaim, H. Tenenbaum, and S. Werner. "Variable Cell Responses to P. gingivalis Lipopolysaccharide." Journal of Dental Research 88, no. 8 (August 2009): 741–45. http://dx.doi.org/10.1177/0022034509341166.

Full text

Abstract:

Porphyromonas gingivalis is a major etiological agent of chronic periodontal diseases, the virulence of which has been attributed to different factors, including lipopolysaccharide (LPS). We investigated the differential responses induced by P. gingivalis LPS stimulation of human umbilical vein endothelial cells and human oral epithelial cells. RT-PCR analysis showed that P. gingivalis LPS used Toll-like receptor 2 (TLR2) to activate epithelial cells and Toll-like receptor 4 (TLR4) to activate endothelial cells. Both cell types were stimulated by P. gingivalis LPS to produce pro-inflammatory cytokines. Cytokine Array assay showed that although patterns of cytokine expression were similar in both cell types, some cytokines were specifically secreted by the endothelial cells, and others were specific to epithelial cells. These results support the idea that the same LPS preparation can act as a TLR2 or TLR4 agonist, depending on TLR expression of the host cell, inducing cytokine profiles that differ according to the cell type.

APA, Harvard, Vancouver, ISO, and other styles

27

Tabeta, Kouich, Kazuhisa Yamazaki, Sachiko Akashi, Kensuke Miyake, Hidefumi Kumada, Toshio Umemoto, and Hiromasa Yoshie. "Toll-Like Receptors Confer Responsiveness to Lipopolysaccharide from Porphyromonas gingivalis in Human Gingival Fibroblasts." Infection and Immunity 68, no. 6 (June 1, 2000): 3731–35. http://dx.doi.org/10.1128/iai.68.6.3731-3735.2000.

Full text

Abstract:

ABSTRACT Gingival fibroblasts produce proinflammatory cytokines in response to lipopolysaccharide (LPS) from periodontopathic bacteria. Recently it has become evident that the human homologue of DrosophilaToll can transduce intracellular signaling by LPS stimulation. Toll-like receptors (TLRs) have been identified in myeloid cells; however, their role in nonmyeloid cells such as gingival fibroblasts has not been fully elucidated. Here, we report that human gingival fibroblasts constitutively express TLR2 and TLR4 and that their levels of expression are increased by stimulation with LPS fromPorphyromonas gingivalis. Upregulated expression of interleukin-6 gene and protein in fibroblasts stimulated with LPS is inhibited by anti-TLR4 antibody. These findings suggest that TLRs may confer responsiveness to LPS in gingival fibroblasts.

APA, Harvard, Vancouver, ISO, and other styles

28

Liu, Sumei, Guojing Liu, Qingxian Luan, Yongping Ma, and Xiaoqian Yu. "Porphyromonas gingivalis Lipopolysaccharide-Induced B Cell Differentiation by Toll-like Receptors 2 and 4." Protein & Peptide Letters 29, no. 1 (January 2022): 46–56. http://dx.doi.org/10.2174/0929866528666211118085828.

Full text

Abstract:

Background: Porphyromonas gingivalis (P. gingivalis) is a pathogenic bacterium widely present in subgingival plaques of patients with periodontitis. It induces periodontitis with bone loss as its main feature by changing the number and composition of symbiotic microorganisms, as well as inducing the natural immune response of the host. However, the mechanism of the latter remains unclear. Objective: This study aims to investigate the effect of P. gingivalis lipopolysaccharide (LPS) on regulatory B cells (Breg) in the occurrence and development of periodontitis. Method: We detected the mRNA levels of IL-10 in B cells under the stimulation of P. gingivalis LPS and/or E. coli LPS, distinguished IL-10-producing cells from different B cell subgroups using flow cytometry. Through toll-like receptor (TLR) knockout mice, the role of TLR2 and TLR4 in this process was also evaluated. Results: Results showed that P. gingivalis stimulated B cells to produce IL-10 via TLR2/4. CD5+B1 subset is the main source of IL-10+Breg cell. Under P. gingivalis LPS stimulation, CD5+IgM+CD93-IL-10+B cell subset increased significantly, which was regulated through TLR2/ 4. Conclusion: The results of this study provides new insights into the immunopathogenic mechanism of P. gingivalis, preliminarily discussed the effect of P. gingivalis on the production of Breg, and present a theoretical foundation for subsequent investigations on the occurrence and development of periodontitis.

APA, Harvard, Vancouver, ISO, and other styles

29

Luan, Chang, Jiaqing Yan, Ning Jiang, Chuang Zhang, Xu Geng, Zhengqiang Li, and Chen Li. "Leuconostoc mesenteroides LVBH107 Antibacterial Activity against Porphyromonas gingivalis and Anti-Inflammatory Activity against P. gingivalis Lipopolysaccharide-Stimulated RAW 264.7 Cells." Nutrients 14, no. 13 (June 22, 2022): 2584. http://dx.doi.org/10.3390/nu14132584.

Full text

Abstract:

Probiotics, active microorganisms benefiting human health, currently serve as nutritional supplements and clinical treatments. Periodontitis, a chronic infectious oral disease caused by Porphyromonas gingivalis (P. gingivalis), activates the host immune response to release numerous proinflammatory cytokines. Here, we aimed to clarify Leuconostoc mesenterica (L. mesenteroides) LVBH107 probiotic effects based on the inhibition of P. gingivalis activities while also evaluating the effectiveness of an in vitro P. gingivalis lipopolysaccharide-stimulated RAW 264.7 cell-based inflammation mode. L. mesenteroides LVBH107 survived at acid, bile salts, lysozyme, and hydrogen peroxide conditions, auto-aggregated and co-aggregated with P. gingivalis, exhibited strong hydrophobicity and electrostatic action, and strongly adhered to gingival epithelial and HT-29 cells (thus exhibiting oral tissue adherence and colonization abilities). Moreover, L. mesenteroides LVBH107 exhibited sensitivity to antibiotics erythromycin, doxycycline, minocycline, ampicillin, and others (thus indicating it lacked antibiotic resistance plasmids), effectively inhibited P. gingivalis biofilm formation and inflammation (in vitro inflammation model), reduced the secretion of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β) and inflammatory mediators (NO and PGE2), and decreased the expression levels of inflammation related genes. Thus, L. mesenterica LVBH107 holds promise as a probiotic that can inhibit P. gingivalis biofilm formation and exert anti-inflammatory activity to maintain oral health.

APA, Harvard, Vancouver, ISO, and other styles

30

Andrian, Elisoa, Daniel Grenier, and Mahmoud Rouabhia. "Porphyromonas gingivalis lipopolysaccharide induces shedding of syndecan-1 expressed by gingival epithelial cells." Journal of Cellular Physiology 204, no. 1 (2005): 178–83. http://dx.doi.org/10.1002/jcp.20287.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Putnins, Edward E., Ali-Reza Sanaie, Qiang Wu, and James D. Firth. "Induction of Keratinocyte Growth Factor 1 Expression by Lipopolysaccharide Is Regulated by CD-14 and Toll-Like Receptors 2 and 4." Infection and Immunity 70, no. 12 (December 2002): 6541–48. http://dx.doi.org/10.1128/iai.70.12.6541-6548.2002.

Full text

Abstract:

ABSTRACT Periodontal disease is a chronic inflammatory condition that is associated with increased concentrations of gram-negative pathogenic bacteria and epithelial cell proliferation. Regulation of this proliferation is poorly understood but is most likely controlled by locally expressed growth factors. Keratinocyte growth factor 1, an epithelium-specific growth factor, is expressed by gingival fibroblasts, and its expression is regulated in a concentration-dependent manner by lipopolysaccharide. In this study, induction of keratinocyte growth factor 1 protein expression was dependent on gingival fibroblast expression of membrane CD14 (mCD14) and Toll-like receptors 2 and 4. Lipopolysaccharides from Escherichia coli and Porphyromonas gingivalis induced membrane expression of CD14 at 1, 3, and 24 h. Specifically, lipopolysaccharide induced low mCD14 expression gingival fibroblasts to express mCD14 at a level consistent with that of high mCD14 expression cells. Functional studies with specific blocking antibodies for CD14 and Toll-like receptors 2 and 4 implicated all of these molecules in signal transduction. The rapid decrease in cell membrane expression of Toll-like receptors 2 and 4 after treatment with lipopolysaccharide was consistent with receptor internalization, and blocking of either of these receptors completely inhibited keratinocyte growth factor 1 protein expression. The transcription factors AP-1 and NF-κB were involved in lipopolysaccharide induction of keratinocyte growth factor 1 mRNA and protein expression. These results suggest that lipopolysaccharide may induce proliferation of periodontal epithelial cells by upregulating keratinocyte growth factor 1 expression via the CD14 and Toll-like receptor signaling pathway.

APA, Harvard, Vancouver, ISO, and other styles

32

Gu, Jian-Yu, Zi-bo Fu, Jia-lu Chen, Yu-Jie Liu, Xian-zi Cao, and Ying Sun. "Endotoxin tolerance induced by Porphyromonas gingivalis lipopolysaccharide alters macrophage polarization." Microbial Pathogenesis 164 (March 2022): 105448. http://dx.doi.org/10.1016/j.micpath.2022.105448.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Kim, Yeon, So-Jeong Kim, Mi-Kyoung Kim, Hyun-Joo Park, Hyung Joon Kim, Soo-Kyung Bae, and Moon-Kyoung Bae. "Porphyromonas gingivalis Lipopolysaccharide Regulates Migration of Vascular Smooth Muscle Cells." International Journal of Oral Biology 41, no. 4 (December 30, 2016): 217–23. http://dx.doi.org/10.11620/ijob.2016.41.4.217.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Choi, Seulggie, Jung Eun Baik, Jun Ho Jeon, Kun Cho, Deog-Gyu Seo, Kee-Yeon Kum, Cheol-Heui Yun, and Seung Hyun Han. "Identification of Porphyromonas gingivalis lipopolysaccharide-binding proteins in human saliva." Molecular Immunology 48, no. 15-16 (September 2011): 2207–13. http://dx.doi.org/10.1016/j.molimm.2011.06.434.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Preshaw, Philip M., Robert E. Schifferle, and John D. Walters. "Porphyromonas gingivalis lipopolysaccharide delays human polymorphonuclear leukocyte apoptosis in vitro." Journal of Periodontal Research 34, no. 4 (May 1999): 197–202. http://dx.doi.org/10.1111/j.1600-0765.1999.tb02242.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Leira, Yago, Ramón Iglesias-Rey, Noemí Gómez-Lado, Pablo Aguiar, Francisco Campos, Francesco D’Aiuto, José Castillo, Juan Blanco, and Tomás Sobrino. "Porphyromonas gingivalis lipopolysaccharide-induced periodontitis and serum amyloid-beta peptides." Archives of Oral Biology 99 (March 2019): 120–25. http://dx.doi.org/10.1016/j.archoralbio.2019.01.008.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Slomiany, Bronislaw L., and Amalia Slomiany. "Leptin suppresses Porphyromonas gingivalis lipopolysaccharide interference with salivary mucin synthesis." Biochemical and Biophysical Research Communications 312, no. 4 (December 2003): 1099–103. http://dx.doi.org/10.1016/j.bbrc.2003.11.035.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Li, Xinyue, Naoko Kato, Masaru Mezawa, Zhengyang Li, Zhitao Wang, Li Yang, Yoko Sasaki, et al. "Transcriptional regulation of bone sialoprotein gene by Porphyromonas gingivalis lipopolysaccharide." Journal of Cellular Biochemistry 110, no. 4 (April 1, 2010): 823–33. http://dx.doi.org/10.1002/jcb.22594.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Kim, Young-Jae, and Sung-Hoon Lee. "Reducing the bioactivity of Tannerella forsythia lipopolysaccharide by Porphyromonas gingivalis." Journal of Microbiology 52, no. 8 (August 2014): 702–8. http://dx.doi.org/10.1007/s12275-014-4324-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Lu, H. K., H. P. Chou, C. L. Li, M. Y. Wang, and L. F. Wang. "Stimulation of Cells Derived from Nifedipine-induced Gingival Overgrowth with Porphyromonas gingivalis, Lipopolysaccharide, and Interleukin-1β." Journal of Dental Research 86, no. 11 (November 2007): 1100–1104. http://dx.doi.org/10.1177/154405910708601115.

Full text

Abstract:

The purpose of this study was to clarify the main contributory factor of nifedipine-induced gingival overgrowth either by Porphyromonas gingivalis lipopolysaccharide ( Pg-LPS) or interleukin-1beta (IL-1β). Human gingival fibroblasts from healthy tissues and nifedipine-induced gingival overgrowth tissues were stimulated with nifedipine, IL-1β, Escherichia coli lipopolysaccharide ( Ec-LPS), and Pg-LPS, and the gene expressions were analyzed by RT-PCR. Analysis of the data showed no strong evidence of a synergistic effect of nifedipine and Pg-LPS on IL-6, connective tissue growth factor (CTGF), and type 1 collagen gene expression of either healthy cells or nifedipine-induced gingival overgrowth cells. Among the three stimulants—IL-1β, Pg-LPS, and Ec-LPS—androgen receptor and IL-6 gene expressions in both the healthy and nifedipine-induced gingival overgrowth groups were strongly up-regulated by the presence of IL-1β only. Furthermore, the responses to IL-1β in the nifedipine-induced gingival overgrowth group were stronger than those of the healthy group. It can be concluded that IL-1β is an important mediator responsible for the higher IL-6 and androgen receptor expression of nifedipine-induced gingival overgrowth cells.

APA, Harvard, Vancouver, ISO, and other styles

41

Nakao, Ryoma, Hidenobu Senpuku, and Haruo Watanabe. "Porphyromonas gingivalis galE Is Involved in Lipopolysaccharide O-Antigen Synthesis and Biofilm Formation." Infection and Immunity 74, no. 11 (September 5, 2006): 6145–53. http://dx.doi.org/10.1128/iai.00261-06.

Full text

Abstract:

ABSTRACT Porphyromonas gingivalis is a crucial component of complex plaque biofilms that form in the oral cavity, resulting in the progression of periodontal disease. To elucidate the mechanism of periodontal biofilm formation, we analyzed the involvement of several genes related to the synthesis of polysaccharides in P. gingivalis. Gene knockout P. gingivalis mutants were constructed by insertion of an ermF-ermAM cassette; among these mutants, the galE mutant showed some characteristic phenotypes involved in the loss of GalE activity. As expected, the galE mutant accumulated intracellular carbohydrates in the presence of 0.1% galactose and did not grow in the presence of galactose at a concentration greater than 1%, in contrast to the parental strain. Lipopolysaccharide (LPS) analysis indicated that the length of the O-antigen chain of the galE mutant was shorter than that of the wild type. It was also demonstrated that biofilms generated by the galE mutant had an intensity 4.5-fold greater than those of the wild type. Further, the galE mutant was found to be significantly susceptible to some antibiotics in comparison with the wild type. In addition, complementation of the galE mutation led to a partial recovery of the parental phenotypes. We concluded that the galE gene plays a pivotal role in the modification of LPS O antigen and biofilm formation in P. gingivalis and considered that our findings of a relationship between the function of the P. gingivalis galE gene and virulence phenotypes such as biofilm formation may provide clues for understanding the mechanism of pathogenicity in periodontal disease.

APA, Harvard, Vancouver, ISO, and other styles

42

Murakami, Yukio, Mamoru Machino, and Seiichiro Fujisawa. "Porphyromonas gingivalis Fimbria-Induced Expression of Inflammatory Cytokines and Cyclooxygenase-2 in Mouse Macrophages and Its Inhibition by the Bioactive Compounds Fibronectin and Melatonin." ISRN Dentistry 2012 (April 1, 2012): 1–7. http://dx.doi.org/10.5402/2012/350859.

Full text

Abstract:

Porphyromonas gingivalis (Pg) fimbriae, in addition to lipopolysaccharide, are involved in the pathogenesis of periodontal disease. At the same time, bioactive compounds such as fibronectin (FN) and melatonin in saliva and gingival crevicular fluid have been reported to exert a preventive effect against periodontitis. Here, we review current knowledge regarding the potent inhibitory effects of FN and melatonin against Pg fimbria-induced induction of proinflammatory cytokines, cyclooxygenase-2 (COX-2) expression, and NF-kappa B activation in mouse macrophages and discuss their possible clinical application for prevention of periodontal diseases induced by oral bacteria.

APA, Harvard, Vancouver, ISO, and other styles

43

Darveau, Richard P., Saman Arbabi, Iris Garcia, Brian Bainbridge, and Ronald V. Maier. "Porphyromonas gingivalis Lipopolysaccharide Is Both Agonist and Antagonist for p38 Mitogen-Activated Protein Kinase Activation." Infection and Immunity 70, no. 4 (April 2002): 1867–73. http://dx.doi.org/10.1128/iai.70.4.1867-1873.2002.

Full text

Abstract:

ABSTRACT Lipopolysaccharide (LPS) is a key inflammatory mediator. It has been proposed to function as an important molecule that alerts the host of potential bacterial infection. Although highly conserved, LPS contains important structural differences among different bacterial species that can significantly alter host responses. For example, LPS obtained from Porphyromonas gingivalis, an etiologic agent for periodontitis, evokes a highly unusual host cell response. Human monocytes respond to this LPS by the secretion of a variety of different inflammatory mediators, while endothelial cells do not. In addition, P. gingivalis LPS inhibits endothelial cell expression of E-selectin and interleukin 8 (IL-8) induced by other bacteria. In this report the ability of P. gingivalis LPS to activate p38 mitogen-activated protein (MAP) kinase was investigated. It was found that p38 MAP kinase activation occurred in response to P. gingivalis LPS in human monocytes. In contrast, no p38 MAP kinase activation was observed in response to P. gingivalis LPS in human endothelial cells or CHO cells transfected with human Toll-like receptor 4 (TLR-4). In addition, P. gingivalis LPS was an effective inhibitor of Escherichia coli-induced p38 MAP kinase phosphorylation in both endothelial cells and CHO cells transfected with human TLR-4. These data demonstrate that P. gingivalis LPS activates the LPS-associated p38 MAP kinase in monocytes and that it can be an antagonist for E. coli LPS activation of p38 MAP kinase in endothelial and CHO cells. These data also suggest that although LPS is generally considered a bacterial component that alerts the host to infection, LPS from P. gingivalis may selectively modify the host response as a means to facilitate colonization.

APA, Harvard, Vancouver, ISO, and other styles

44

Sato, Keiko, Nobuo Kido, Yukitaka Murakami, Charles I. Hoover, Koji Nakayama, and Fuminobu Yoshimura. "Lipopolysaccharide biosynthesis-related genes are required for colony pigmentation of Porphyromonas gingivalis." Microbiology 155, no. 4 (April 1, 2009): 1282–93. http://dx.doi.org/10.1099/mic.0.025163-0.

Full text

Abstract:

The periodontopathic bacterium Porphyromonas gingivalis forms pigmented colonies when incubated on blood agar plates as a result of accumulation of μ-oxo haem dimer on the cell surface. Gingipain–adhesin complexes are responsible for production of μ-oxo haem dimer from haemoglobin. Non-pigmented mutants (Tn6-5, Tn7-1, Tn7-3 and Tn10-4) were isolated from P. gingivalis by Tn4351 transposon mutagenesis [Hoover & Yoshimura (1994), FEMS Microbiol Lett 124, 43–48]. In this study, we found that the Tn6-5, Tn7-1 and Tn7-3 mutants carried Tn4351 DNA in a gene homologous to the ugdA gene encoding UDP-glucose 6-dehydrogenase, a gene encoding a putative group 1 family glycosyltransferase and a gene homologous to the rfa gene encoding ADP heptose-LPS heptosyltransferase, respectively. The Tn10-4 mutant carried Tn4351 DNA at the same position as that for Tn7-1. Gingipain activities associated with cells of the Tn7-3 mutant (rfa) were very weak, whereas gingipain activities were detected in the culture supernatants. Immunoblot and mass spectrometry analyses also revealed that gingipains, including their precursor forms, were present in the culture supernatants. A lipopolysaccharide (LPS) fraction of the rfa deletion mutant did not show the ladder pattern that was usually seen for the LPS of the wild-type P. gingivalis. A recombinant chimera gingipain was able to bind to an LPS fraction of the wild-type P. gingivalis in a dose-dependent manner. These results suggest that the rfa gene product is associated with biosynthesis of LPS and/or cell-surface polysaccharides that can function as an anchorage for gingipain–adhesin complexes.

APA, Harvard, Vancouver, ISO, and other styles

45

Napa, Kiran, Andrea C. Baeder, Jeffrey E. Witt, Sarah T. Rayburn, Madison G. Miller, Blake W. Dallon, Jonathan L. Gibbs, et al. "LPS from P. gingivalis Negatively Alters Gingival Cell Mitochondrial Bioenergetics." International Journal of Dentistry 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/2697210.

Full text

Abstract:

Objective. Oral inflammatory pathologies are linked to increased oxidative stress, thereby partly explaining their relevance in the etiology of systemic disorders. The purpose of this work was to determine the degree to which LPS from Porphyromonas gingivalis, the primary pathogen related to oral inflammation, altered gingival mitochondrial function and reactive oxygen species generation. Methods. Human gingival fibroblast (HGF-1) cells were treated with lipopolysaccharide of P. gingivalis. Mitochondrial function was determined via high-resolution respirometry. Results. LPS-treated HGF-1 cells had significantly higher mitochondrial complex IV and higher rates of mitochondrial respiration. However, this failed to translate into greater ATP production, as ATP production was paradoxically diminished with LPS treatment. Nevertheless, production of the reactive H2O2 was elevated with LPS treatment. Conclusions. LPS elicits an increase in gingival cell mitochondria content, with a subsequent increase in reactive oxygen species production (i.e., H2O2), despite a paradoxical reduction in ATP generation. These findings provide an insight into the nature of oxidative stress in oral inflammatory pathologies.

APA, Harvard, Vancouver, ISO, and other styles

46

Lee, Hae Jin, So Jung Lee, Sung-Kwon Lee, Bong-Keun Choi, and Dong-Ryung Lee. "Magnolia kobus Extract Inhibits Periodontitis-Inducing Mediators in Porphyromonas gingivalis Lipopolysaccharide-Activated RAW 264.7 Cells." Current Issues in Molecular Biology 45, no. 1 (January 6, 2023): 538–54. http://dx.doi.org/10.3390/cimb45010036.

Full text

Abstract:

Periodontitis, a disease caused by inflammation of oral bacteria, contributes to the loss of alveolar bone and destruction of connective tissues. Porphyromonas gingivalis, a Gram-negative bacterium, is known to possess important pathogenic factors for periodontal disease. In this study, we investigated the anti-periodontitis effects of Magnolia kobus extract (MKE) and magnolin as a component of Magnolia kobus (MK) in murine macrophage RAW 264.7 cells stimulated with Porphyromonas gingivalis lipopolysaccharide (LPS). Effects of MKE and magnolin on the mechanism of RAW 264.7 cellular inflammation were determined by analyzing nitric oxide (NO) production and Western blot protein expression (n = 3). MKE/magnolin inhibited NO production without affecting cell survival. MKE/magnolin treatment inhibited LPS-induced pro-inflammatory cytokines, expression levels of matrix metalloproteinases (MMPs such as MMP-1, 3, 8, 9, and 13), and protein levels of inflammatory mediators (such as TNF-α, IL-1β, and mPGES-1). MKE/magnolin also suppressed NF-κB activation by inhibiting the TLR4 signaling pathway. These findings suggest that MKE has a therapeutic effect on inflammatory periodontal disease caused by oral bacterium P. gingivalis and that magnolin is a major functional component in the anti-inflammatory effect of MKE.

APA, Harvard, Vancouver, ISO, and other styles

47

Yang, Kai, Shuo Xu, Hongmei Zhao, Lingshuang Liu, Xiaofang Lv, Fang Hu, Lei Wang, and Qiuxia Ji. "Hypoxia and Porphyromonas gingivalis-lipopolysaccharide synergistically induce NLRP3 inflammasome activation in human gingival fibroblasts." International Immunopharmacology 94 (May 2021): 107456. http://dx.doi.org/10.1016/j.intimp.2021.107456.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Kang, Wenyan, Zhekai Hu, and Shaohua Ge. "Healthy and Inflamed Gingival Fibroblasts Differ in Their Inflammatory Response to Porphyromonas gingivalis Lipopolysaccharide." Inflammation 39, no. 5 (August 15, 2016): 1842–52. http://dx.doi.org/10.1007/s10753-016-0421-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Zaric, Svetislav, Charles Shelburne, Richard Darveau, Derek J. Quinn, Sinéad Weldon, Clifford C. Taggart, and Wilson A. Coulter. "Impaired Immune Tolerance to Porphyromonas gingivalis Lipopolysaccharide Promotes Neutrophil Migration and Decreased Apoptosis." Infection and Immunity 78, no. 10 (August 2, 2010): 4151–56. http://dx.doi.org/10.1128/iai.00600-10.

Full text

Abstract:

ABSTRACT Periodontitis, a chronic inflammatory disease of the tissues supporting the teeth, is characterized by an exaggerated host immune and inflammatory response to periopathogenic bacteria. Toll-like receptor activation, cytokine network induction, and accumulation of neutrophils at the site of inflammation are important in the host defense against infection. At the same time, induction of immune tolerance and the clearance of neutrophils from the site of infection are essential in the control of the immune response, resolution of inflammation, and prevention of tissue destruction. Using a human monocytic cell line, we demonstrate that Porphyromonas gingivalis lipopolysaccharide (LPS), which is a major etiological factor in periodontal disease, induces only partial immune tolerance, with continued high production of interleukin-8 (IL-8) but diminished secretion of tumor necrosis factor alpha (TNF-α) after repeated challenge. This cytokine response has functional consequences for other immune cells involved in the response to infection. Primary human neutrophils incubated with P. gingivalis LPS-treated naïve monocyte supernatant displayed a high migration index and increased apoptosis. In contrast, neutrophils treated with P. gingivalis LPS-tolerized monocyte supernatant showed a high migration index but significantly decreased apoptosis. Overall, these findings suggest that induction of an imbalanced immune tolerance in monocytes by P. gingivalis LPS, which favors continued secretion of IL-8 but decreased TNF-α production, may be associated with enhanced migration of neutrophils to the site of infection but also with decreased apoptosis and may play a role in the chronic inflammatory state seen in periodontal disease.

APA, Harvard, Vancouver, ISO, and other styles

50

Sidarningsih, Sidarningsih, Indeswati Diyatri, Reinaya Tifa Pratiwi, Jihan Hijriya Nabilla, Yuliati Yuliati, and Rini Devijanti Ridwan. "Epigallocatechin gallate Mucoadhesive Gingival Patch as Potential Biomaterial to Regulate Macrophage and Lymphocyte Cells in Periodontitis: A Review." Indonesian Journal of Dental Medicine 5, no. 1 (June 27, 2022): 32–36. http://dx.doi.org/10.20473/ijdm.v5i1.2022.32-36.

Full text

Abstract:

Background: Periodontitis is a periodontal disease that affects more than 743 million peopleworldwide and causes damage to the periodontal ligament and alveolar bone. One of the bacteriathat can cause periodontitis is Porphyromonas gingivalis (P.gingivalis). P. gingivalis has virulence factors that can damage the periodontal tissue. Treatment of periodontitis is in the form of non- surgical therapy such as scaling and root planning and some cases, doxycycline can be given as adjunctive therapy after scaling and root planing. Epigallocatechin gallate (EGCG) is one of the catechins found in green tea and has anti-bacterial properties. Purpose: The study aimed to describe the potency of the mucoadhesive gingival patch with EGCG green tea against the number of macrophage cells and lymphocyte cells during periodontitis through narrative review. Review: Mucoadhesive gingiva patch loaded with EGCG has the advantages such as maintaining drug bioavailability, non-invasive, and optimizing drug distribution. Using a mucoadhesive gingiva patch with EGCG can reduce macrophage and lymphocyte cells by inhibiting lipopolysaccharide, a virulence factor of P. gingivalis. Inhibited lipopolysaccharide will inhibit pro-inflammatory cytokines such as TNF-α and IL-6. Macrophage and lymphocyte cells will reduce due to the inhibition of pro inflammatory cytokines. Conclusion: Mucoadhesive gingiva patch with EGCG green tea potentially to decreased macrophage and lymphocyte cells in periodontitis.

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!