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Relevant bibliographies by topics / Porphyromonas gingivalis lipopolysaccharide

Academic literature on the topic 'Porphyromonas gingivalis lipopolysaccharide'

Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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Journal articles on the topic "Porphyromonas gingivalis lipopolysaccharide"

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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Dissertations / Theses on the topic "Porphyromonas gingivalis lipopolysaccharide"

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Al-Qutub, Montaser Nazmi. "Lipopolysaccharide lipid A structural heterogeneity of Porphyromonas gingivalis /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/6383.

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Huck, Olivier. "Infection et stimulation de cellules endothéliales par Porphyromonas gingivalis et son lipopolysaccharide : lien entre maladies parodontales et athérosclérose." Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ021.

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Depuis plusieurs années, l’influence des pathologies parodontales sur certaines pathologies systémiques, notamment les maladies cardio-vasculaires et l’athérosclérose apparait de plus en plus évidente. Dans notre étude, nous nous sommes intéressés à l’évaluation des effets induits par Porphyromonas gingivalis, une des principales bactéries parodontopathogènes, et son lipopolysaccharide sur les cellules endothéliales, qui forment une interface entre le flux sanguin et la paroi vasculaire, d’où un rôle important dans l’initiation et le développement de la plaque d’athérome. Nous avons surtout ciblé les effets induits sur la cathepsine B, une protéase impliquée dans le développement de la plaque d’athérome, et sur l’inflammasome, un complexe impliqué dans la production d’IL-1beta. Les résultats de nos travaux montrent que l’infection par Porphyromonas gingivalis et la stimulation par son LPS sont capables d’induire une augmentation de l’activité enzymatique de la cathepsine B, ceci suivant différentes cinétiques. Dans les deux cas, ces augmentations d’activité se font sans modifications de la synthèse d’ARNm, ni de la concentration protéique de l’enzyme. Nos résultats démontrent également que l’infection par Porphyromonas gingivalis entraine une augmentation de l’expression ARN de l’inflammasome NLRP3, mais celle ci n’est pas observée au niveau protéique du fait d’un processus de protéolyse de la protéine NLRP3 suite à l’infection. Dans un deuxième temps, nous avons développé un modèle de parodontite expérimentale, fiable et reproductible, nous permettant d’envisager une expérimentation in vivo afin d’observer les interactions à distance entre maladies parodontales et athérosclérose sur dessouris apolipoprotéine-E -/-
Periodontal diseases have been linked to systemic diseases especially cardiovascular diseases and atherosclerosis. In our study, we investigated the effects induced by an infection with Porphyromonas gingivalis, a major periodontal pathogen, and stimulation by its lipopolysaccharide on endothelial cells at the interface between the inner part of arteries and blood flow. We focused on the effects induced on cathepsin B, a protease involved in atherosclerosis and on the activation of inflammasome, an intracellular complex linked to secretion of IL-1beta. Results showed that infection with Porphyromonas gingivalis and stimulation by its lipopolysaccharide increase enzymatic activity of cathepsin B with different kinetics. These modifications are observed without any modifications of RNAm expression and protein concentration. We also showed that infection with Porphyromonas gingivalis increases RNAm expression of NLRP3 but this increase at the RNAm level is not associated with an increase of the protein concentration due to an induced proteolysis. Furthermore, we developed a reliable model of experimental periodontitis that will be used to analyze interactions between periodontitis and systemic diseases in vivo, especially in apolipoprotein-E -/- mice

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Bainbridge, Brian W. "Generation and function of Porphyromonas gingivalis lipid A heterogeneity /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/6394.

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Zhou, Lili [Verfasser]. "Porphyromonas gingivalis lipopolysaccharides affect gingival stem/progenitor cells attributes through NF-κB, but not Wnt/β-catenin pathway / Lili Zhou." Kiel : Universitätsbibliothek Kiel, 2018. http://d-nb.info/1173703454/34.

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Herath, Mudiyanselage Thanuja Darshani Kumari Herath. "A systems biological study on heterogeneous Porphyromonas gingivalis lipopolysaccharides: human gingivalfibroblasts interaction : molecular mechanisms and implications inperiodontal pathogenesis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hub.hku.hk/bib/B50162615.

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Porphyromonas gingivalis is a keystone periodontopathogen and its lipopolysacharide (LPS) is strongly associated with periodontal disease. A long-standing controversy occurs on the role of P. gingivalis LPS in induction of innate host response in different cell types. It has recently been found that P. gingivalis LPS displays remarkable heterogeneity with both tetra- (LPS1435/1449) and penta-acylated (LPS1690) lipid A structures. However, the potential effects of heterogeneous structures of P. gingivalis LPS on modulating host innate responses in human gingival fibrobalsts (HGFs) - the most abundant cells in gingiva remain unclear. To fulfill this research gap, a comprehensive study on the P. gingivalis LPS-HGFs interations was undertaken. The effects of P. gingivalis LPS1435/1449 and LPS1690 on the expression profiles of pro-inflammatory cytokines were investigated (Chapter III). P. gingivalis LPS1690 (not LPS1435/1449) significantly upregulated the expression of IL-6, IL-8 and TNF-α, suggesting that P. gingivalis LPS may differentially modulate the expression of pro-inflammatory cytokines. The effects of P. gingivalis LPS on the expression of MMPs 1-3 and TIMP-1, and regulation of MMP-3 were then determined (Chapter IV). P. gingivalis LPS1690 markedly induced MMP-3 expression through p38 MAPK and ERK signal pathways, whereas TIMP-1 was greatly upregulated by P. gingivalis LPS1435/1449. These findings suggest that P. gingivalis LPS heterogeneity may differentially modulate the expression and regulation of MMP-3. Based on these findings, the involvements of TLR2/4 and the downstream signaling pathways were explored (Chapter V). P. gingivalis LPS1690 induced TLR4 expression, whereas TLR2 was upregulated by P. gingivalis LPS1435/1449. NF-κB pathway played a dominant role in P. gingivalis LPS1690-induced expression of IL-6 and IL-8. These findings suggest that the two isoforms of P. gingivalis LPS critically interact with TLR2 and TLR4, and may determine the subsequent activation of signal transduction cascades that differentially modulate immuno-inflammatory response. P. gingivalis could thereby evade innate host defense and contribute to periodontal pathogenesis. To obtain a holistic profile of heterogeneous P. gingivalis LPS-HGFs interactions, a systems biology-based study through proteomics, metabolomics and bioinformatics approaches was undertaken (Chapter VI). Pro-inflammatory proteins (e.g. Cyclophilin, Annexins, IL-6 and Cathepsins) were induced by P. gingivalis LPS1690. In contrast, anti-inflammatory proteins (e.g. ANXA1, ANXA2 and Gal-1) were upregulated by P. gingivalis LPS1435/1449. P. gingivalis LPS1690 also induced antioxidant defense molecules like MnSOD and PRDXs. Secretomic analysis showed that immuno-inflammatory mediators, extra-cellular proteases and matrix proteins were differentially modulated by the two isoforms of P. gingivalis LPS as well. These findings demonstrate that host responses such as immuno-inflammatory activity, oxidative stress and anti-oxidant defense may be differentially modulated and regulated by the heterogeneous P. gingivalis LPS. Further study shows that P. gingivalis LPS1435/1449 and LPS1690 differentially modulate oxidative stress response and antioxidant expression, and differential regulation of MnSOD could be a critical determinant of periodontal homeostasis (Chapter VII). The present findings may bring new insight into the molecular mechanisms of periodontal pathogenesis. Targeting the mechanisms of shift in lipid A structures of P. gingivalis LPS may be a potential strategy to develop novel approaches to control and prevent periodontal diseases.
published_or_final_version
Dentistry
Doctoral
Doctor of Philosophy

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Dixon, Douglas Raymond. "Lipid A heterogeneity within Porphyromonas gingivalis and other oral bacteria : effect of lipid A content on hTLR4 utilization and E-selectin expression /." Thesis, Connect to this title online; UW restricted, 2005. http://hdl.handle.net/1773/6385.

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Gross, Jane Elizabeth. "Local and systemic host immune responses to Porphyromonas gingivalis A7436 infection in a subcutaneous tissue chamber in untreated and lipopolysaccharide-treated mice." 1999. http://catalog.hathitrust.org/api/volumes/oclc/48199463.html.

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Lan-YunChang and 張藍云. "Effects of Recombinant Thrombomodulin Domain 1 in Porphyromonas gingivalis Lipopolysaccharide-Induced Osteoclastogenesis." Thesis, 2019. http://ndltd.ncl.edu.tw/handle/8q83xt.

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Huang, Kun-Che, and 黃堃哲. "HBD2-Overexpression decreases BMSC Proinflammatory Cytokine Expression of BMSC after Porphyromonas gingivalis Lipopolysaccharide Stimulation." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/2ghv7x.

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碩士
國立陽明大學
口腔生物研究所
106
Periodontitis is a common oral inflammatory disease caused by bacterial infection which leads to destruction of periodontal tissues. Successful periodontal regenerative therapy requires reduction of bacteria-related pathogenic factors and promotion of tissue regeneration. Porphyromonas gingivalis (Pg) is a major pathogen of periodontitis. Pg lipopolysaccharide (LPS) induces the production of proinflammatory cytokines, such as interleukin (IL)-1β (IL-1β), IL-6, and IL-8, and plays an important role in Pg’s pathogenic mechanism. Human β-defensin 2 (hBD2) is an important antimicrobial peptide of innate immune system. Previous studies indicated that hBD2 is effective against Pg. The positive charge of hBD2 potentially can neutralize the negative-charged LPS. Stem cell therapy is an effective treatment strategy for regenerative therapies including the regeneration of periodontal defects. Application of hBD2-overexpressing bone marrow stem cell (hBD2/BMSC) in treatment of bacteria-contaminated bone defect shows excellent antimicrobial and bone regenerative effects. Thus, hBD2/BMSC shows great potential in periodontal regenerative therapies. It has been reported that LPS induces production of proinflammatory cytokines in bone marrow stem cells. However, the effects of Pg-LPS on hBD2/BMSC may be different. We hypothesized that hBD2 produced by hBD2/BMSC can neutralize Pg-LPS and reduce the expression of proinflammatory cytokines from cells stimulated by Pg-LPS. The purpose of this study was to determine the Pg-LPS-induced proinflammatory cytokine expression of hBD2/BMSC. Human bone marrow stem cells (3A6) overexpressing red fluorescent protein (RFP) or hBD2, namely RFP/3A6 and hBD2/3A6, were produced by lentiviral infection method. The red fluorescence of RFP/3A6 was verified under fluorescent microscope. The secreted hBD2 from hBD2/3A6 was quantified by enzyme-linked immunosorbent assay (ELISA). Various concentrations of Pg-LPS (0, 0.1, 1 μg/ml) were used to treat RFP/3A6 and hBD2/3A6. The induced expression of proinflammatory cytokines (IL-1β、IL-6, and IL-8) of RFP/3A6 and hBD2/3A6 was determined by quantitative PCR and compared. The results indicated that the secretion of hBD2 can be increased through repeated lentiviral infection strategy. Pg-LPS stimulation dose-dependently increase the expression of proinflammatory cytokines (IL-1β、IL-6, and IL-8) of RFP/3A6 and hBD2/3A6. The trend of expression increase is significantly smaller in hBD2/3A6 when compared with RFP/3A6. When treated with Pg-LPS (0.1 or 1 μg/ml))，hBD2/3A6 showed lower expression of proinflammatory cytokines (IL-1β、IL-6, and IL-8) than RFP/3A6. In conclusion, the overexpression of hBD2 of BMSCs can lower the Pg-LPS-induced expression of proinflammatory cytokines. The phenomenon may reduce the local inflammation during periodontal regenerative therapy and benefit the periodontal regeneration

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Tsai, Man-chin, and 蔡嫚今. "Diallyl sulfide diminished the Porphyromonas gingivalis lipopolysaccharide stimulated pro-inflammatory cytokine expression and NF-κB activation in gingival fibroblasts." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/16465942363879007682.

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碩士
國防醫學院
牙醫科學研究所
100
Introduction: Periodontitis is a chronic infection and inflammatory disease, which is a multi-factorial disease, risks for moderate to severe periodontitis that have been identified include specific pathogenic bacteria (such as Porphyromonas gingivalis), environment, behavior, and certain other systemic conditions. Studies showed that the fibroblasts actively participate in immune and inflammatory events in periodontal diseases. Future strategies for the prevention and treatment of periodontal diseases should biologically regulate fibroblast activities. Garlic is a common flavor food since ancient times. Garlic is composed with a variety of sulfur-based compounds. The most important components of garlic are allicin and scordinin which has a strong ability of oxide-reduction, anti-bacterial, anti-inflammatory, anti-cancer, and improving the immune system. Purpose of this study is to examine the role of garlic extract in reducing periodontal inflammation by using the gingival fibroblast cultures and the animal models of experimental periodontitis. Materials and Methods: In this study, we examined the anti-inflammatory effects of diallyl sulfide on P. g LPS-induced inflammation in human gingival fibroblasts. The cytotoxicity effects of diallyl sulfide on the cell was measured by MTS assay with/without LPS stimulation. The effects of diallyl sulfide on LPS-stimulated the mRNA expressions of TNF-α, IL-1β, and IL-6 were investigated by RT-PCR. The inhibitory effects of diallyl sulfide on NF-κB activation, TNF-α and IL-1β expression were examined by immunocytochemical staining (ICC). Results: In this study, we demonstrated that diallyl sulfide in the concentration of 0, 1, 2, 3 mM combined with LPS (1 g/ml) did not affect HGFs’ survival. The LPS-stimulated mRNA expressions of TNF-α, IL-1β, and IL-6 in HGFs were inhibited when pretreated with diallyl sulfide. The LPS-stimulated NF-κB activation and protein expressions of TNF-α, IL-1β in HGFs were repressed when pretreated with diallyl sulfide. Conclusion: In this study, we found and demonstrated that diallyl sulfide could reduce the periodontal inflammation in the gingival fibroblast cultures.

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Books on the topic "Porphyromonas gingivalis lipopolysaccharide"

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Andreou, Vana. Resveratrol mediated reversal of aryl hydrocarbon and porphyromonas gingivalis lipopolysaccharide induced inhibition of osteogenesis in vitro. 2002.

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Book chapters on the topic "Porphyromonas gingivalis lipopolysaccharide"

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Ishikawa, Taichi, Yuko Ohara-Nemoto, Shihoko Tajika, Minoru Sasaki, and Shigenobu Kimura. "The production of secretory leukocyte protease inhibitor from gingival epithelial cells in response to Porphyromonas gingivalis lipopolysaccharides." In Interface Oral Health Science 2009, 275–76. Tokyo: Springer Japan, 2010. http://dx.doi.org/10.1007/978-4-431-99644-6_77.

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Pritchard, Anna Barlach, Zsolt Fabian, Clare L. Lawrence, Glyn Morton, StJohn Crean, and Jane E. Alder. "An Investigation into the Effects of Outer Membrane Vesicles and Lipopolysaccharide of Porphyromonas gingivalis on Blood-Brain Barrier Integrity, Permeability, and Disruption of Scaffolding Proteins in a Human in vitro Model." In Advances in Alzheimer’s Disease. IOS Press, 2022. http://dx.doi.org/10.3233/aiad220044.

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Background: The effects of the key pathogens and virulence factors associated with gum disease such as Porphyromonas gingivalis (P. gingivalis) on the central nervous system is of great interest with respect to development of neuropathologies and hence therapeutics and preventative strategies. Chronic infections and associated inflammation are known to weaken the first line of defense for the brain, the blood-brain barrier (BBB). Objective: The focus of this study is to utilize an established human in vitro BBB model to evaluate the effects of P. gingivalis virulence factors lipopolysaccharide (LPS) and outer membrane vesicles (OMVs) on a primary-derived human model representing the neurovascular unit of the BBB. Methods: Changes to the integrity of the BBB after application of P. gingivalis LPS and OMVs were investigated and correlated with transport of LPS. Additionally, the effect of P. gingivalis LPS and OMVs on human brain microvascular endothelial cells in monolayer was evaluated using immunofluorescence microscopy. Results: The integrity of the BBB model was weakened by application of P. gingivalis LPS and OMVs, as measured by a decrease in electrical resistance and a recovery deficit was seen in comparison to the controls. Application of P. gingivalis OMVs to a monoculture of human brain microvascular endothelial cells showed disruption of the tight junction zona occludens protein (ZO-1) compared to controls. Conclusion: These findings show that the integrity of tight junctions of the human BBB could be weakened by association with P. gingivalis virulence factors LPS and OMVs containing proteolytic enzymes (gingipains).

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Qian, Xueshen, Shuang Zhang, Lian Duan, Fengchun Yang, Kun Zhang, Fuhua Yan, and Song Ge. "Periodontitis Deteriorates Cognitive Function and Impairs Neurons and Glia in a Mouse Model of Alzheimer’s Disease." In Advances in Alzheimer’s Disease. IOS Press, 2022. http://dx.doi.org/10.3233/aiad220042.

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Background: Although periodontitis is reportedly associated with increased cognitive decline in Alzheimer’s disease, the mechanisms underlying this process remain unknown. Porphyromonas gingivalis lipopolysaccharide (P.g-LPS) is an endotoxin associated with periodontal disease. Objective: We investigated the effect of periodontitis on learning capacity and memory of amyloid-β protein precursor (AβPP)/presenilin (PS1) transgenic mice along with the mechanisms underlying these effects. Methods: Mice were randomly assigned to three groups, namely AβPP/PS1 (control), P.g-LPS Injection, and P.g-LPS Injection + Ligation. Mice from the P.g-LPS Injection group were injected with P.g-LPS in the periodontal tissue three times per week for 8 weeks, while mice from the P.g-LPS Injection + Ligation group were injected with P.g-LPS and subjected to ligation of the gingival sulcus of the maxillary second molar. Results: Expression of gingival proinflammatory cytokines as well as alveolar bone resorption in P.g-LPS-injected and ligatured mice was increased compared to that in control mice. Mice in the P.g-LPS Injection + Ligation group exhibited cognitive impairment and a significant reduction in the number of neurons. Glial cell activation in the experimental groups with significantly increased amyloid-β (Aβ) levels was more pronounced relative to the control group. Induction of periodontitis was concurrent with an increase in cyclooxygenase-2, inducible nitric oxide synthase, AβPP, and beta-secretase 1 expression and a decrease in A disintegrin and metalloproteinase domain-containing protein 10 expression. Conclusion: These findings indicated that periodontitis exacerbated learning and memory impairment in AβPP/PS1 mice and augmented Aβ and neuroinflammatory responses. Our study provides a theoretical basis for risk prediction and early intervention of Alzheimer’s disease and periodontitis.

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Cornelia Nelwan, Sindy, Ricardo Adrian Nugraha, Anang Endaryanto, Frisma Dewi, Yonna Dwi Swastika, Udijanto Tedjosasongko, and Seno Pradopo. "Correlation between Salivary Lipopolysaccharide of Porphyromonas gingivalis with Circulatory Immunoglobulin-E and Immunoglobulin-G4 in Periodontally Healthy Children with House Dust Mite Allergy." In Gingival Disease - A Professional Approach for Treatment and Prevention. IntechOpen, 2019. http://dx.doi.org/10.5772/intechopen.81113.

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