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
6
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
10
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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Thanomchard, Thanastha, and Thanastha Thanomchard. "Evaluation of Porphyromonas gingivalis lipopolysaccharide on the expression of inflammatory mediators leading to bone resorption." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/7gtt6b.
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Yang, Tsai-Shan, and 楊彩姍. "Effects of High Glucose Culture and Advanced Glycation End Productson Porphyromonas gingivalis Lipopolysaccharide Induced IL-6 and IL-8 Expressions in Gingival Fibroblasts." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/95348815775492620677.
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碩士國防醫學院
牙醫科學研究所
101
Background & aims: Periodontitis is a chronic infection and inflammatory disease, in which inflammation in the periodontal tissues by the long term presence of the dental plaque. Study showed that there are some specific pathogenic bacteria such as Porphyromonas gingivalis may actively participate immune and inflammatory events in periodontal disease. Diabetes is a group of metabolic diseases in which a person has high blood sugar (hyperglycemia). Hyperglycemia results in the formation of advanced glycation end-products (AGEs). These AGEs act to “prime” endothelial cells and monocytes, making them more susceptible to stimuli that induce the cells to produce inflammatory mediators. Accumulation of AGEs in the plasma and tissues of diabetic patients has been linked to diabetic complications. Periodontitis develops as a result of host-mediated inflammation to periodontal pathogens. Hyperglycemia and AGEs have been hypothesized as the etiologic factors of diabetic periodontitis. AGEs have been identified as a class of pro-inflammatory mediators through RAGE/NF-κB pathway. Aim of study was to investigate that the effect of high glucose culture and advanced glycation end products (AGEs) on Porphyromonas gingivalis LPS induced IL-6 and IL-8 expressions in human gingival fibroblasts Methods: Cytotoxicity of AGEs and Porphyromonas gingivalis LPS on HGFs were measured by MTS assay. The expression of IL-6 and IL-8 of cells was examined by ELISA. The activation of NF-κB was evaluated by immunocytochemistry. Results: AGEs alone had no influence on the survival rates of HGFs either cultured in low or high glucose; however, P.g LPS affected the cell survival at the dose of 1000 ng/ml when cultured in high glucose. Protein expression for IL-6 and IL-8 of HGFs were increased by AGEs and P.g LPS treatment, while the combined treatment of AGEs (25 μg/ml) and P.g LPS (1000 ng/ml) significantly increased the protein expressions of IL-6 and IL-8. Conclusions: This study demonstrated that AGEs and P.g LPS synergistically stimulate the expressions of IL-6 and IL-8 of HGFs in high glucose culture. Whether it may through the activation of NF-κB.
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Wen, Wanchun, and 文萬鈞. "Epigallocatechin-3-gallate Decreases the Porphyromonas gingivalis Lipopolysaccharide-induced Matrix Metalloproteinase-1 Production in Human Gingival Fibroblast Through the Inhibition of Interleukin-6." Thesis, 2012. http://ndltd.ncl.edu.tw/handle/81335266331500990685.
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碩士國防醫學院
牙醫科學研究所
100
BACKGROUND: Green tea is produced from Camellia sinensis. And the most effective in reacting with reaction oxygen species and anti-inflammation is (-)-epigallocatechin-3-gallate, EGCG. Periodontal disease is an inflammatory disease may damage surrounding tissue and bone, causing tooth loss. In periodontitis, bacteria and their products, lipopolysaccharide, LPS can penetrate gingival connective tissue and induce a local inflammatory response that leads to periodontal bone resorption. Human gingival fibroblast are the most proportion in connective tissue, under lipopolysaccharide stimulation, HGFs will continuously releasing pro-inflammatory cytokines. Periodontitis is also in relation of host-immune systems. P. gingivalis LPS stimulated human gingival fibroblasts and found increased IL-6 and MMP-1 production. EGCG treatment showed anti-inflammation and anti-degradation in several studies. Decreased IL-6 synthesis and MMPs production were reported. PURPOSE: The aims of the study were 1) to evaluate the ameliorative effect of EGCG on the P.g LPS-enhanced MMP-1 production in human gingival fibroblasts, and 2) to further elucidate the role of IL-6 on ameliorative effect. RESULTS: Significantly increased MMP-1 amount was observed in HGFs after the stimulations of P.g LPS with a dose dependent manner. However, EGCG significantly reduced the LPS-enhanced MMP-1 amount. Significantly increased IL-6 mRNA expression was observed in HGFs after P.g LPS treatment. The IL-6 protein production was also increased after P.g LPS treatments. However, EGCG reduced the LPS-enhanced IL-6 mRNA and protein expressions. P.g LPS significantly increased MMP-1 protein production; however, the anti-IL-6 antibody inhibited the LPS-stimulated MMP-1. In addition, IL-6 treatment significantly enhanced the MMP-1 production, with a dose dependent manner. CONCLUSION: In the present study, EGCG inhibited the P.g LPS-induced MMP-1 production in HGFs through the regulation of IL-6. Thus may provide a possible prevention and treatment for periodontal disease through the anti-degradation ability.
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Yeh, Kuei-Chih, and 葉桂枝. "Effect of Porphyromonas gingivalis lipopolysaccharide on theregulation of OPG/RANKL and Interleukin-6 in the serum ofsimulating murine model of postmenopausal osteoporosis." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/94131325892074017877.
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碩士臺北醫學大學
牙醫學系
93
Periodontitis is a chronic inflammatory disease which results in the breakdown of tooth supporting structures, especially alveolar bone destruction. Deep periodontal pocket, attachment level loss, and alveolar bone loss are found under clinical examination. Porphyromonas gingivalis (P. gingivalis), a black-pigmented gram-negative anaerobic bacterial rods, is a vital pathogen for adult periodontitis. P. gingivalis has been proved to contribute to bone resorption in many vivo studies. However, unlike the clear relationship between osteoporosis and tooth loss, controversy still exists concerning the association between osteopenia/opteoporosis and the periodontal pathogen. The purpose of the present study is to clarify the etiologic relationship of P. gingivalis lipopolysaccharide (P. gingivalis LPS) and the expression of OPG, RANKL, IL-6 in the serum of postmenopausal osteoporosis mice. Injection of Escherichia coli LPS (E. coli LPS) was need as the control. Ninty 10-week old ICR female mice were divided into ovariectomized group (experimental group) and sham-operation group (control group). After operation 4 weeks, we collect the serum as baseline. 100 µg P. gingivalis LPS and E. coli LPS were separately injected into the peritoneum of experimental group (30 mice) and control group (30 mice). Subsequently, we collected the serum 1,3,6,24 and 48 hours after the injection of both LPS. Then the concentrations of IL-6, OPG and RANKL of serum will be estimated by using sandwich ELISA. The femur bone was dissected for TRAP stain analysis. Besides, 4 weeks after operation, 15 experimental mice and 15 control mice was sacrificed for TRAP stain to compare lipopolysaccharide effect. Mann-Whitney U test was applied to study the difference of OPG, RANKL, OPG/RANKL ratio, IL-6 between P. gingivalis LPS and E. coli LPS. Wilcoxon signed rank test was used to study the difference of OPG, RANKL, OPG/RANKL ratio, IL-6 between each time interval and baseline in group. The strength of correlations between IL-6 and OPG, RANKL, OPG/RANKL ratio at each time interval in group were determined by Spearman rank correlation coefficients. The difference of TRAP positive cell count in the specimen among was compared by using Kruskal-Wallis test. Results with p< 0.05 were defined statistically different. In the injection of P. gingivalis LPS of experimental and control group, OPG/RANKL ratio decreased at 3 hours (p< 0.05), then trended to rising tendency. IL-6 rose at 1、3 hours (p< 0.05). Besides, the changes of OPG, RANKL, OPG/RANKL ratio, IL-6 were greater in injection of E. coli LPS than P. gingivalis LPS. There is stronger TRAP positive cells distribution in experimental group than control group (p< 0.05). No matter single booster of P. gingivalis LPS or E. coli LPS did not effect the expression of TRAP positive cells. It should be noticed that only single shot of bacterial LPS was applied in this animal model. P. gingivalis LPS directly effected the expression of IL-6, but not OPG/RANKL system. It indicated that OPG/RANKL ratio of experimental group injected with P. gingivalis LPS might also be regulated by a more complex system. Removal of ovary did not effect the expression of IL-6; our data also indicated there were no correlation of IL-6, expression of OPG, RANKL, and OPG/RANKL ratio. In addition, the stimulatory effect of E. coli LPS was stronger than P. gingivalis LPS.
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Chou, Hsuan-Po, and 周宣伯. "Expression of androgen receptor, interleukin-6, and Th1 / Th2 cytokines in the cells derived from nifedipine induced gingival overgrowth tissue stimulated with Porphyromonas gingivalis lipopolysaccharide and interleukin-1b." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/59019680354304530074.
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碩士臺北醫學大學
口腔復健醫學研究所
92
From immunostaining results of Th1/Th2 of nifedipine induced gingival overgrowth（NIGO）tissues and other periodontal tissues in 2001, a significant expression of androgen receptor（AR）could be observed. Using these results in vivo, we addressed the hypothesis that AR’s improvement and Th1 cytokine’s expression might be the pathogenic factors to NIGO. The present study extended above clinical trials in vivo. Gingival fibroblast from healthy, H（n=4, age: 30-39 y/o）tissues and NIGO（n=4, age: 48-65 y/o）tissues were handled from periodontal surgery area and put into cell culture. After third generation, pre-determined IL-1β and LPS of Porphyromonas gingivalis were used to stimulated sample cells for 48 hours. The concentration of the pre-determined extract was 10 μg/ml for LPS endotoxins and 10 ng/ml for IL-1β, respectively. These gingival fibroblasts were used as our control group in this experiment. Expression of IL-2、IL-4 and IL-6 extracted from supernatant were measured by ELISA. On the other hand, Cell layer extracted from pellet were analyzed by PCR to detect expression level of mRNA of IL-2、IL-4、IL-6 and AR. After 48 hours induction, the expression of IL-2 and IL-4 is under detetable value in this study either in supernatant or cell layer. Increased expression was detectable in the part of AR and IL-6 through mRNA level and ELISA. We used Gel Doc software to semi-quantify our PCR product under ultraviolet and studied the statistic difference between groups by Mann-Whitney U software. Results with p<0.05 showed that the amount of AR and IL-6 form these two groups（H and NIGO）were increased after IL-1β induction for 48 hours. However, the difference of AR and IL-6 between control group and experimental group with LPS stimulated was not remarkable. The information from using Spearman Rank Correlation Coeffienct for IL-6 and AR studies also showed no significant results while stimulated by different drugs. Besides bacteria, pathogenic mechanism of periodontal disease could not only induced inflammation but also evoke lots of cytokines to participate in. Through above experiments, we discovered NIGO cells were more sensitive to the induction of IL-1b than by P. gingivalis - LPS. It implies that in the treatment of NIGO, traditional periodontal treatment adjusted with anti-inflammatory drugs and biological agents can be conducted to inhibit both the effects of periodontal pathogen and pre-inflammatory cytokine on NIGO gingival fibroblast.
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Doyle, Catherine Jane. "Azithromycin suppresses P. gingivalis LPS induced pro-inflammatory cytokine and chemokine production (IL-6, IL-8, MCP-1 & GRO) by human gingival fibroblasts in vitro." Thesis, 2014. http://hdl.handle.net/2440/84847.
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Azithromycin is a macrolide antibiotic that is well known for its antibacterial properties, as well as possessing potential anti-inflammatory and immune modulating effects. This antibiotic has therefore been widely used in medicine for treating conditions ranging from inflammatory pulmonary diseases to dermatologic skin conditions. It has also been shown to be an effective antibiotic against most common periodontal pathogens and is used as an adjunct to treat periodontitis, a condition with bacterial aetiology and an inflammatory pathogenesis. Furthermore, periodontal case studies report regeneration of alveolar bone accompanied by significant reductions in inflammation have been achieved with azithromycin. The mechanisms however, by which these are achieved in the periodontium are largely unknown. This study aimed to determine the potential anti-inflammatory effect of azithromycin on cytokine and chemokine production by healthy human gingival fibroblasts (HGFs) that were stimulated by Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS). HGFs were isolated from healthy gingiva collected from three donors. The effects of azithromycin at concentrations ranging from 0.1 to 10 μg/mL were tested. Cytokine and chemokine protein levels were assessed using the Luminex® multiplex immunoassay. P. gingivalis LPS induced cytokine/chemokine (IL-6, IL-8, MCP-1 and GRO) protein production in HGFs was suppressed by azithromycin at all concentrations tested, and in all three donors. Suppression by azithromycin of IL-6, IL-8, MCP-1 and GRO P. gingivalis LPS protein induction in HGF was statistically significant when all donor results were collated (p<0.05). This study demonstrates that azithromycin suppresses P. gingivalis LPS induced cytokine/chemokine protein production in HGFs, which may explain some of the clinical benefits observed with the adjunctive use of azithromycin in the treatment of periodontitis.Thesis (D.Clin.Dent.) -- University of Adelaide, School of Dentistry, 2014