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Letteratura scientifica selezionata sul tema "Gingivalis"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 25 aprile 2022

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Articoli di riviste sul tema "Gingivalis"

1

Waller, Tobias, Laura Kesper, Josefine Hirschfeld, Henrik Dommisch, Johanna Kölpin, Johannes Oldenburg, Julia Uebele et al. "Porphyromonas gingivalis Outer Membrane Vesicles Induce Selective Tumor Necrosis Factor Tolerance in a Toll-Like Receptor 4- and mTOR-Dependent Manner". Infection and Immunity 84, n. 4 (8 febbraio 2016): 1194–204. http://dx.doi.org/10.1128/iai.01390-15.

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Abstract (sommario):

Porphyromonas gingivalisis an important member of the anaerobic oral flora. Its presence fosters growth of periodontal biofilm and development of periodontitis. In this study, we demonstrated that lipophilic outer membrane vesicles (OMV) shed fromP. gingivalispromote monocyte unresponsiveness to liveP. gingivalisbut retain reactivity to stimulation with bacterial DNA isolated fromP. gingivalisor AIM2 ligand poly(dA·dT). OMV-mediated tolerance ofP. gingivalisis characterized by selective abrogation of tumor necrosis factor (TNF). Neutralization of interleukin-10 (IL-10) during OMV challenge partially restores monocyte responsiveness toP. gingivalis; full reactivity toP. gingivaliscan be restored by inhibition of mTOR signaling, which we previously identified as the major signaling pathway promoting Toll-like receptor 2 and Toll-like receptor 4 (TLR2/4)-mediated tolerance in monocytes. However, despite previous reports emphasizing a central role of TLR2 in innate immune recognition ofP. gingivalis, our current findings highlight a selective role of TLR4 in the promotion of OMV-mediated TNF tolerance: only blockade of TLR4—and not of TLR2—restores responsiveness toP. gingivalis. Of further note, OMV-mediated tolerance is preserved in the presence of cytochalasin B and chloroquine, indicating that triggering of surface TLR4 is sufficient for this effect. Taking the results together, we propose thatP. gingivalisOMV contribute to local immune evasion ofP. gingivalisby hampering the host response.

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2

Huang, George T. J., Daniel Kim, Jonathan K. H. Lee, Howard K. Kuramitsu e Susan Kinder Haake. "Interleukin-8 and Intercellular Adhesion Molecule 1 Regulation in Oral Epithelial Cells by Selected Periodontal Bacteria: Multiple Effects of Porphyromonas gingivalis via Antagonistic Mechanisms". Infection and Immunity 69, n. 3 (1 marzo 2001): 1364–72. http://dx.doi.org/10.1128/iai.69.3.1364-1372.2001.

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Abstract (sommario):

ABSTRACT Interaction of bacteria with mucosal surfaces can modulate the production of proinflammatory cytokines and adhesion molecules produced by epithelial cells. Previously, we showed that expression of interleukin-8 (IL-8) and intercellular adhesion molecule 1 (ICAM-1) by gingival epithelial cells increases following interaction with several putative periodontal pathogens. In contrast, expression of IL-8 and ICAM-1 is reduced after Porphyromonas gingivalis ATCC 33277 challenge. In the present study, we investigated the mechanisms that govern the regulation of these two molecules in bacterially infected gingival epithelial cells. Experimental approaches included bacterial stimulation of gingival epithelial cells by either a brief challenge (1.5 to 2 h) or a continuous coculture throughout the incubation period. The kinetics of IL-8 and ICAM-1 expression following brief challenge were such that (i) secretion of IL-8 by gingival epithelial cells reached its peak 2 h following Fusobacterium nucleatum infection whereas it rapidly decreased within 2 h after P. gingivalis infection and remained decreased up to 30 h and (ii) IL-8 and ICAM-1 mRNA levels were up-regulated rapidly 2 to 4 h postinfection and then decreased to basal levels 8 to 20 h after infection with either Actinobacillus actinomycetemcomitans, F. nucleatum, or P. gingivalis. Attenuation of IL-8 secretion was facilitated by adherent P. gingivalis strains. The IL-8 secreted from epithelial cells after F. nucleatum stimulation could be down-regulated by subsequent infection with P. gingivalisor its culture supernatant. Although these results suggested that IL-8 attenuation at the protein level might be associated with P. gingivalis proteases, the Arg- and Lys-gingipain proteases did not appear to be solely responsible for IL-8 attenuation. In addition, while P. gingivalis up-regulated IL-8 mRNA expression, this effect was overridden when the bacteria were continuously cocultured with the epithelial cells. The IL-8 mRNA levels in epithelial cells following sequential challenge with P. gingivalis andF. nucleatum and vice versa were approximately identical and were lower than those following F. nucleatum challenge alone and higher than control levels or those following P. gingivalis challenge alone. Thus, together with the protease effect, P. gingivalis possesses a powerful strategy to ensure the down-regulation of IL-8 and ICAM-1.

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3

Suzuki, Mitsuo, Toshizo Toyama, Kiyoko Watanabe, Haruka Sasaki, Shuta Sugiyama, Fumihiko Yoshino, Ayaka Yoshida et al. "Ameliorating Effects of Jixueteng in a Mouse Model of Porphyromonas gingivalis-Induced Periodontitis: Analysis Based on Gingival Microcirculatory System". Natural Product Communications 13, n. 12 (dicembre 2018): 1934578X1801301. http://dx.doi.org/10.1177/1934578x1801301230.

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Abstract (sommario):

Jixueteng, the dried stem of Spatholobus suberectus Dunn (Leguminosae), is a traditional Chinese herbal medicine that promotes blood circulation and can be used to treat blood stasis. In this study, we aimed to investigate the potential of Jixueteng as a preventive and therapeutic drug for periodontitis. We investigated the inhibitory effects of Jixueteng on Porphyromonas gingivalis ( P. gingivalis)-induced gingival circulatory disturbances in mice. Seventy-two male C57BL/6N mice (4-week-old) were randomly divided into the following four groups of 12 mice each. Group 1 served as the P. gingivalis noninfected control (control group). Group 2 was administered Jixueteng extract in drinking water to P. gingivalis noninfected control mice. Group 3 was infected orally with P. gingivalis; and group 4 was administered Jixueteng extract in drinking water and then infected with P. gingivalis. To evaluate the effect of Jixueteng on gingival microcirculation systems, we examined gingival blood flow (GBF) in oral microcirculation in vivo in a mouse model of periodontitis. Gingival reactive hyperemia (GRH) was determined using laser Doppler flowmetry. GRH was elicited by the release of occlusive gingival compression by the laser Doppler probe (diameter 1.0 mm) for 1 min. GRH was estimated by basal blood flow, maximum response (Peak), the time taken for the maximum response to fall to one half (T1/2) and increased total amount of blood flow (Mass). Furthermore, to determine the effect of an oral application of P. gingivalis and/or Jixueteng on GBF and gingival microvessel ultrastructure, morphological analysis of gingival microvessels was performed by using a vascular resin cast model. Administration of Jixueteng to P. gingivalis-infected animals significantly reduced GRH, especially T1/2 and Mass, compared to that in P. gingivalis-infected animals. Alternatively, in the morphological analysis, reduction of the gingival capillary network which resulted from P. gingivalis-infection was improved by Jixueteng administration. Since Jixueteng ameliorates P. gingivalis infection-induced gingival circulatory disturbance, it may be useful in the treatment of P. gingivalis-induced periodontitis.

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4

Griffen, Ann L., Mitzi R. Becker, Sharon R. Lyons, Melvin L. Moeschberger e Eugene J. Leys. "Prevalence of Porphyromonas gingivalisand Periodontal Health Status". Journal of Clinical Microbiology 36, n. 11 (1998): 3239–42. http://dx.doi.org/10.1128/jcm.36.11.3239-3242.1998.

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Abstract (sommario):

Periodontitis is a common, progressive disease that eventually affects the majority of the population. The local destruction of periodontitis is believed to result from a bacterial infection of the gingival sulcus, and several clinical studies have provided evidence to implicate Porphyromonas gingivalis. If P. gingivalis is a periodontal pathogen, it would be expected to be present in most subjects with disease and rarely detected in subjects with good periodontal health. However, in most previous studies, P. gingivalis has not been detected in the majority of subjects with disease, and age-matched, periodontally healthy controls were not included for comparison. The purpose of the study reported here was to compare the prevalence of P. gingivalis in a group with periodontitis to that of a group that is periodontally healthy. A comprehensive sampling strategy and a sensitive PCR assay were used to maximize the likelihood of detection. The target sequence for P. gingivalis-specific amplification was the transcribed spacer region within the ribosomal operon. P. gingivalis was detected in only 25% (46 of 181) of the healthy subjects but was detected in 79% (103 of 130) of the periodontitis group (P < 0.0001). The odds ratio for being infected with P. gingivalis was 11.2 times greater in the periodontitis group than in the healthy group (95% confidence interval, 6.5 to 19.2). These data implicate P. gingivalisin the pathogenesis of periodontitis and suggest that P. gingivalis may not be a normal inhabitant of a periodontally healthy dentition.

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5

Bao, X., R. Wiehe, H. Dommisch e A. S. Schaefer. "Entamoeba gingivalis Causes Oral Inflammation and Tissue Destruction". Journal of Dental Research 99, n. 5 (5 febbraio 2020): 561–67. http://dx.doi.org/10.1177/0022034520901738.

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Abstract (sommario):

A metagenomics analysis showed a strongly increased frequency of the protozoan Entamoeba gingivalis in inflamed periodontal pockets, where it contributed the second-most abundant rRNA after human rRNA. This observation and the close biological relationship to Entamoeba histolytica, which causes inflammation and tissue destruction in the colon of predisposed individuals, raised our concern about its putative role in the pathogenesis of periodontitis. Histochemical staining of gingival epithelium inflamed from generalized severe chronic periodontitis visualized the presence of E. gingivalis in conjunction with abundant neutrophils. We showed that on disruption of the epithelial barrier, E. gingivalis invaded gingival tissue, where it moved and fed on host cells. We validated the frequency of E. gingivalis in 158 patients with periodontitis and healthy controls by polymerase chain reaction and microscopy. In the cases, we detected the parasite in 77% of inflamed periodontal sites and 22% of healthy sites; 15% of healthy oral cavities were colonized by E. gingivalis. In primary gingival epithelial cells, we demonstrated by quantitative real-time polymerase chain reaction that infection with E. gingivalis but not with the oral bacterial pathogen Porphyromonas gingivalis strongly upregulated the inflammatory cytokine IL8 (1,900 fold, P = 2 × 10–4) and the epithelial barrier gene MUC21 (8-fold, P = 7 × 10–4). In gingival fibroblasts, we showed upregulation of the collagenase MMP13 (11-fold, P = 3 × 10–4). Direct contact of E. gingivalis to gingival epithelial cells inhibited cell proliferation. We indicated the strong virulence potential of E. gingivalis and showed that the mechanisms of tissue invasion and destruction are similar to the colonic protozoan parasite E. histolytica. In conjunction with abundant colonization of inflamed periodontal sites and the known resistance of Entamoeba species to neutrophils, antimicrobial peptides, and various antibiotics, our results raise the awareness of this protozoan as a potential and, to date, underrated microbial driver of destructive forms of periodontitis.

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6

Darveau, Richard P., Carol M. Belton, Robert A. Reife e Richard J. Lamont. "Local Chemokine Paralysis, a Novel Pathogenic Mechanism for Porphyromonas gingivalis". Infection and Immunity 66, n. 4 (1 aprile 1998): 1660–65. http://dx.doi.org/10.1128/iai.66.4.1660-1665.1998.

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Abstract (sommario):

ABSTRACT Periodontitis, which is widespread in the adult population, is a persistent bacterial infection associated with Porphyromonas gingivalis. Gingival epithelial cells are among the first cells encountered by both P. gingivalis and commensal oral bacteria. The chemokine interleukin 8 (IL-8), a potent chemoattractant and activator of polymorphonuclear leukocytes, was secreted by gingival epithelial cells in response to components of the normal oral flora. In contrast, P. gingivalis was found to strongly inhibit IL-8 accumulation from gingival epithelial cells. Inhibition was associated with a decrease in mRNA for IL-8. Antagonism of IL-8 accumulation did not occur in KB cells, an epithelial cell line that does not support high levels of intracellular invasion by P. gingivalis. Furthermore, a noninvasive mutant of P. gingivalis was unable to antagonize IL-8 accumulation. Invasion-dependent destruction of the gingival IL-8 chemokine gradient at sites of P. gingivaliscolonization (local chemokine paralysis) will severely impair mucosal defense and represents a novel mechanism for bacterial colonization of host tissue.

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7

Liu, Chengcheng, Kendall Stocke, Zackary R. Fitzsimonds, Lan Yakoumatos, Daniel P. Miller e Richard J. Lamont. "A bacterial tyrosine phosphatase modulates cell proliferation through targeting RGCC". PLOS Pathogens 17, n. 5 (20 maggio 2021): e1009598. http://dx.doi.org/10.1371/journal.ppat.1009598.

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Abstract (sommario):

Tyrosine phosphatases are often weaponized by bacteria colonizing mucosal barriers to manipulate host cell signal transduction pathways. Porphyromonas gingivalis is a periodontal pathogen and emerging oncopathogen which interferes with gingival epithelial cell proliferation and migration, and induces a partial epithelial mesenchymal transition. P. gingivalis produces two tyrosine phosphatases, and we show here that the low molecular weight tyrosine phosphatase, Ltp1, is secreted within gingival epithelial cells and translocates to the nucleus. An ltp1 mutant of P. gingivalis showed a diminished ability to induce epithelial cell migration and proliferation. Ltp1 was also required for the transcriptional upregulation of Regulator of Growth and Cell Cycle (RGCC), one of the most differentially expressed genes in epithelial cells resulting from P. gingivalis infection. A phosphoarray and siRNA showed that P. gingivalis controlled RGCC expression through Akt, which was activated by phosphorylation on S473. Akt activation is opposed by PTEN, and P. gingivalis decreased the amount of PTEN in epithelial cells. Ectopically expressed Ltp1 bound to PTEN, and reduced phosphorylation of PTEN at Y336 which controls proteasomal degradation. Ltp-1 induced loss of PTEN stability was prevented by chemical inhibition of the proteasome. Knockdown of RGCC suppressed upregulation of Zeb2 and mesenchymal markers by P. gingivalis. RGCC inhibition was also accompanied by a reduction in production of the proinflammatory cytokine IL-6 in response to P. gingivalis. Elevated IL-6 levels can contribute to periodontal destruction, and the ltp1 mutant of P. gingivalis incited less bone loss compared to the parental strain in a murine model of periodontal disease. These results show that P. gingivalis can deliver Ltp1 within gingival epithelial cells, and establish PTEN as the target for Ltp1 phosphatase activity. Disruption of the Akt1/RGCC signaling axis by Ltp1 facilitates P. gingivalis-induced increases in epithelial cell migration, proliferation, EMT and inflammatory cytokine production.

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8

Okuda, K., e I. Takazoe. "The Role of Bacteroides Gingivalis in Periodontal Disease". Advances in Dental Research 2, n. 2 (novembre 1988): 260–68. http://dx.doi.org/10.1177/08959374880020021001.

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The microbial flora in adult advanced periodontitis lesions is comprised of Gram-negative rods, with Bacteroides gingivalis as one of the major representatives. This review deals with biological properties of surface antigens, hemagglutinin (attachment factor), and capsular structure of B. gingivalis. Sera containing high IgG antibody levels to B. gingivalis enhanced the complement-mediated bactericidal activity in vitro, although the susceptibility to complement-mediated lysis differed among B. gingivalis strains. The protective effect of immunization against B. gingival is infection was examined in hamsters in which cotton threads had been tied to the gingival margins of the mandibular first molar. Repeated oral topical application of hyper-immune sera against B. gingivalis resulted in effective elimination of the organisms from the periodontal lesions in the experimental animals.

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9

Zhou, Yun, Maryta Sztukowska, Qian Wang, Hiroaki Inaba, Jan Potempa, David A. Scott, Huizhi Wang e Richard J. Lamont. "Noncanonical Activation of β-Catenin by Porphyromonas gingivalis". Infection and Immunity 83, n. 8 (1 giugno 2015): 3195–203. http://dx.doi.org/10.1128/iai.00302-15.

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Abstract (sommario):

Porphyromonas gingivalisis an established pathogen in periodontal disease and an emerging pathogen in serious systemic conditions, including some forms of cancer. We investigated the effect ofP. gingivalison β-catenin signaling, a major pathway in the control of cell proliferation and tumorigenesis. Infection of gingival epithelial cells withP. gingivalisdid not influence the phosphorylation status of β-catenin but resulted in proteolytic processing. The use of mutants deficient in gingipain production, along with gingipain-specific inhibitors, revealed that gingipain proteolytic activity was required for β-catenin processing. The β-catenin destruction complex components Axin1, adenomatous polyposis coli (APC), and GSK3β were also proteolytically processed byP. gingivalisgingipains. Cell fractionation and Western blotting demonstrated that β-catenin fragments were translocated to the nucleus. The accumulation of β-catenin in the nucleus followingP. gingivalisinfection was confirmed by immunofluorescence microscopy. A luciferase reporter assay showed thatP. gingivalisincreased the activity of the β-catenin-dependent TCF/LEF promoter.P. gingivalisdid not increase Wnt3a mRNA levels, a finding consistent withP. gingivalis-induced proteolytic processing causing the increase in TCF/LEF promoter activity. Thus, our data indicate thatP. gingivaliscan induce the noncanonical activation of β-catenin and disassociation of the β-catenin destruction complex by gingipain-dependent proteolytic processing. β-Catenin activation in epithelial cells byP. gingivalismay contribute to a proliferative phenotype.

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10

Chin, Yu-Tang, Meng-Ti Hsieh, Chi-Yu Lin, Po-Jan Kuo, Yu-Chen S. H. Yang, Ya-Jung Shih, Hsuan-Yu Lai et al. "2,3,5,4′-Tetrahydroxystilbene-2-O-β-glucoside Isolated from Polygoni Multiflori Ameliorates the Development of Periodontitis". Mediators of Inflammation 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/6953459.

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Periodontitis, a chronic infection by periodontopathic bacteria, induces uncontrolled inflammation, which leads to periodontal tissue destruction. 2,3,5,4′-Tetrahydroxystilbene-2-O-beta-glucoside (THSG), a polyphenol extracted from Polygoni Multiflori, reportedly has anti-inflammatory properties. In this study, we investigated the mechanisms of THSG on thePorphyromonas gingivalis-induced inflammatory responses in human gingival fibroblasts and animal modeling of ligature-induced periodontitis. Human gingival fibroblast cells were treated with lipopolysaccharide (LPS) extracted fromP. gingivalisin the presence of resveratrol or THSG to analyze the expression of TNF-α, IL-1β, and IL-6 genes. Increased AMP-activated protein kinase (AMPK) activation and SirT1 expression were induced by THSG. Treatment of THSG decreased the expression of LPS-induced inflammatory cytokines, enhanced AMPK activation, and increased the expression of SirT1. In addition, it suppressed the activation of NF-κB when cells were stimulated withP. gingivalisLPS. The anti-inflammatory effect of THSG and P. Multiflori crude extracts was reproduced in ligature-induced periodontitis animal modeling. In conclusion, THSG inhibited the inflammatory responses ofP. gingivalis-stimulated human gingival fibroblasts and ameliorated ligature-induced periodontitis in animal model.

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Più fonti

Tesi sul tema "Gingivalis"

1

Hoppe, Tatjana [Verfasser]. "Maligne Transformation gingivaler Epithelzellen durch Porphyromonas gingivalis / Tatjana Hoppe". Bonn : Universitäts- und Landesbibliothek Bonn, 2017. http://d-nb.info/1140525883/34.

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2

Lobos, Matthei Ignacio Felipe. "Regulación de survivina en células epiteliales gingivales infectadas por Porphyromonas gingivalis". Tesis, Universidad de Chile, 2014. http://www.repositorio.uchile.cl/handle/2250/117229.

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Abstract (sommario):

Memoria para optar el título de Bioquímico
La periodontitis crónica es una enfermedad de etiología infecciosa, caracterizada por la respuesta inflamatoria e inmune exacerbada por parte del hospedero que produce la destrucción de tejidos de soporte del diente. Actualmente, se postula que para el establecimiento de esta patología se produce una sucesión ecológica desde una comunidad microbiana asociada a salud hacia una asociada a enfermedad periodontal. En esta sucesión es imprescindible la presencia de ciertos patógenos que faciliten el remodelamiento de la microbiota oral y la progresión hacia enfermedad, siendo Porphyromonas gingivalis un patógeno clave en este proceso. P. gingivalis es una bacteria anaerobia estricta capaz de invadir y permanecer al interior de células epiteliales gingivales. Interesantemente, la infección por P. gingivalis produce una mayor viabilidad celular, mediante la modulación de proteínas relacionadas con apoptosis. Se ha sugerido que la proteína inhibidora de la apoptosis, survivina, podría contribuir a la inhibición de la apoptosis mediada por P. gingivalis; sin embargo, su participación en este proceso no está completamente dilucidada. En esta memoria de título se estudió si P. gingivalis es capaz de modular los niveles de survivina en la línea celular de epitelio gingival OKF6/TERT2 y si esta modulación está relacionada con el grado de virulencia de la bacteria. Para ello, se infectaron células OKF6/TERT2 utilizando dos cepas de referencia y un aislado clínico, cada una con diferente virulencia. Luego, se determinaron los niveles de proteína y transcrito de survivina a tiempos tempranos y tardíos post-invasión, mediante Western blot y RT-PCR. Los resultados obtenidos indican que P. gingivalis es capaz de disminuir los niveles de survivina y que esta modulación podría estar relacionada con la virulencia de la bacteria. Sin embargo, la disminución de survivina no estaría relacionada directamente con la inhibición de apoptosis que genera la infección por P. gingivalis
Chronic periodontitis is an infectious disease characterized by an exacerbated inflammatory and immune response by the host, which causes the destruction of the tooth supporting tissues. Nowadays, it is assumed that for the onset of this pathology an ecological succession from a bacterial community associated to health, to one associated with periodontal disease is produced. In this succession, the presence of certain pathogens facilitate the remodeling of the oral microbiota and the consequent progression to disease, being Porphyromonas gingivalis a key pathogen in this process. P. gingivalis is a strict anaerobic bacterium capable of invading and persisting within gingival epithelial cells. Interestingly, infection by P. gingivalis produce an increase in the viability of these cells by modulation of apoptosis related proteins. It has been suggested that the apoptosis inhibitory protein, survivin, could contribute to the inhibition of apoptosis mediated by P. gingivalis; however, its participation in this process is still unknown. In this work, we studied whether P. gingivalis is capable of modulate survivin levels in gingival epithelial cells OKF6/TERT2 and if this modulation is related to bacterial virulence. To achieve this goals we infected OKF6/TERT2 cells with two reference strains and one clinical isolate, each with different virulence. Survivin protein and transcript levels were determined at early and late post-infection times by Western blot and RT-PCR. The results of this work indicated that P. gingivalis is capable of decreasing survivin levels and this modulation could be related to virulence features of the bacterium. Nevertheless, survivin decrease would not be directly related to the inhibition of apoptosis induced by P. gingivalis

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3

Bugueño, Valdebenito Isaac Maximiliano. "Caracterización de aislados clínicos de Porphyromonas gingivalis y su efecto en la viabilidad de células epiteliales gingivales". Tesis, Universidad de Chile, 2014. http://www.repositorio.uchile.cl/handle/2250/130110.

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Trabajo de Investigación Requisito para optar al Título de Cirujano Dentista
La periodontitis es una enfermedad infecciosa multifactorial, caracterizada por una respuesta inflamatoria exacerbada que produce la destrucción de las estructuras que dan soporte al diente, incluyendo la encía, el ligamento periodontal, el cemento radicular y el hueso alveolar. Para la iniciación de las periodontitis, se requiere la presencia de una comunidad bacteriana subgingival compleja en la cual coexisten diversos géneros y especies microbianas. Dentro de las especies del complejo rojo de Socransky que contribuyen a la etiología de la enfermedad periodontal, está Porphyromonas gingivalis (P. gingivalis). P. gingivalis es una bacteria Gram negativo que tendría especial relevancia en la progresión de la periodontitis. Entre los factores de virulencia de P. gingivalis se encuentran el lipopolisacárido (LPS), las fimbrias y el antígeno K o cápsula, los cuales están involucrados en el proceso de infección. La expresión de estos factores de virulencia por parte de la bacteria, puede variar de manera importante entre individuos, generando una respuesta distinta en los tejidos infectados, como en células epiteliales gingivales. Se ha descrito que P. gingivalis puede invadir las células epiteliales de la encía y modular diferentes vías de señalización que generen inhibición de la activación del sistema inmune e inhibición de la apoptosis celular. En este trabajo, se evaluaron características de la envoltura celular, y propiedades macro y microscópicas de aislados clínicos de P. gingivalis y cepas de referencia, y se evaluó su efecto sobre la viabilidad de células epiteliales gingivales. De esta manera, se analizaron parámetros macromorfológicos de las cepas en medios sólido y líquido. Se evaluó la capacidad de formación de biopelículas, la carga superficial (mediante ensayos de unión a citocromo C y ensayos de hidrofobicidad), se estudió la presencia de cápsula (tinción con tinta china) y caracterizó los perfiles electroforéticos del LPS. Finalmente, se estudió la viabilidad y el nivel de apoptosis de células epiteliales gingivales infectadas por 9 dos cepas virulentas de referencia y 7 aislados clínicos de P. gingivalis, utilizando la línea celular OKF6/TERT2. Estos ensayos fueron realizados en tiempos tempranos, intermedios y tardíos de infección. Nuestros resultados mostraron diferencias en el crecimiento entre aislados clínicos de individuos sanos comparados con enfermos, tanto en medio sólido como en medio líquido. En la mayoría de los aislados clínicos se observó presencia de cápsula. Además, todos formaron más biopelículas que las cepas de referencia, y no se encontraron diferencias significativas entre las muestras de pacientes sanos y enfermos. Adicionalmente, la mayoría de los aislados clínicos presentó una mayor carga superficial que las cepas de referencias. Nuestros resultados también mostraron que todos los aislados clínicos y cepas de referencia de P. gingivalis fueron capaces de invadir células OKF6/TERT2. Adicionalmente, observamos que algunos aislados clínicos aumentaron significativamente la viabilidad celular a tiempos tempranos y tardíos de infección, incluso más que la cepa W50 descrita como una cepa muy virulenta y altamente invasiva. En síntesis, nuestros resultados indican que existen diferencias macromorfológicas y de envoltura celular entre aislados clínicos de P. gingivalis provenientes de individuos sanos y enfermos y que la infección por P. gingivalis mantiene o aumenta la viabilidad en la línea celular derivada de epitelio gingival OKF6/TERT2, como consecuencia de la modulación de la apoptosis. También, observamos que éste fenómeno es dependiente de la virulencia de la cepa. La virulencia se relaciona con características de la envoltura celular y con la presencia de ciertos componentes específicos. Estos aislados clínicos más virulentos podrían estar asociados a cuadros clínicos más agresivos.

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4

Loomer, Peter Michael. "The direct effects of Porphyromonas gingivalis 2561 on bone formation and mineral resorption in vitro". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ27685.pdf.

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5

Houalet-Jeanne, Sylvie. "Etude in-vitro de l'internalisation de Porphyromonas gingivalis dans la cellule pariétale gingivale". Rennes 1, 2001. http://www.theses.fr/2001REN1B085.

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Porphyromonas gingivalis (P. Gingivalis) est décrit comme l'un des pathogènes majeurs de la maladie parodontale. Il est également impliqué dans l'étiologie de pathologies systémiques. A ce jour, les mécanismes précis de son pouvoir de virulence gardent d'importantes zones d'ombre. Le travail présenté ici, s'applique à confirmer le potentiel invasif de la bactérie face à la cellule hôte, et à préciser son devenir dans la cellule épithéliale. L'utilisation de différents marqueurs sur un modèle in vitro, nous a permis de détecter P. Gingivalis au sein de cellules épithéliales de lignée KB en Microscopie Confocale, et d'analyser divers aspects de l'adhérence et de l'internalisation. Parallèlement, nous employons les techniques de culture sur gélose au sang, en enceinte anaérobie.

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6

Meuric, Vincent. "Virulence de Porphyromonas gingivalis". Rennes 1, 2008. http://www.theses.fr/2008REN1B197.

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"Porphyromonas gingivalis est une bactérie anaérobie stricte responsable des maladies parodontales. La respiration et la régulation des gènes de virulence restent inconnues. Ce travail explore la chaîne respiratoire et montre l'aérotolérance de la bactérie. Les résultats affirment la capacité de transmission aéroportée et inter individus par des mécanismes activant des gènes de résistance au stress oxydatif tel que "tpx" sous la dépendance d'OsyR régulateur transcriptionnel. Après une analyse de la littérature sur les principaux gènes de virulence, hémagglutinines et gingipaïnes, les études expérimentales ont montré que l'oxygène atmosphérique n'influence pas leur expression. Par contre, la coagrégation "in vitro" avec "T. Denticola", autre parodontopathogène, entraîne la surespression de "hagA", "rgpA" et "kgp" et par ce phénomène favorise le développement de la maladie parodontale. "

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7

Palm, Eleonor. "Inflammatory responses of gingival fibroblasts in the interaction with the periodontal pathogen Porphyromonas gingivalis". Doctoral thesis, Örebro universitet, Institutionen för hälsovetenskap och medicin, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-38660.

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8

Maley, Janette. "Genetic studies on Porphyromonas gingivalis W83". Thesis, University of Leicester, 1994. http://hdl.handle.net/2381/35395.

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Until recently molecular biological approaches to the study of putative virulence factors of the oral pathogen Porphyromonas gingivalis were limited. This was due to the absence of a genetic system which could facilitate the production of isogenic mutant derivatives. Among the many components produced, the capsule is believed to be of particular importance in the pathogenicity of P. gingivalis. In order to identify mutants lacking capsular polysaccharide, purified capsular material from P. gingivalis W83 was used to generate capsule-specific antisera. However, these antisera contained antibodies which recognised lipopolysaccharide. The use of polymyxin B-agarose was found to be useful in the removal of LPS-reactive material. Capsular polysaccharide was purified further and shown to be free of detectable LPS. A system for conjugal transfer of plasmid DNA from Escherichia coli to P. gingivalis was developed. This method was then used for the introduction of the suicide-vector R751::Tn4351?4 into P. gingivalis. Examination of a number of P. gingivalis Tn4351 mutants demonstrated the presence of multiple copies of Tn4351 in the chromosome of the mutants. Recovery of plasmid pNJR12 from P. gingivalis transconjugants led to the isolation of IS 1126. This insertion sequence was present in the chromosome of all strains of P. gingivalis examined but absent from other members of the genus. The amino acid sequence of the major open reading frame (ORF1) was derived from the nucleotide sequence of IS 1126. ORF1 contained the conserved motifs displayed by the transposase proteins of IS-elements belonging to the IS4 family.

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9

Singh, Umadatt. "The adherence properties of Bacteroides gingivalis". Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/31013.

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A Bacteroides gingivalis adhesin mediating attachment to red blood cells and buccal epithelial cells was isolated, cloned and characterized. The isolation procedure involved gentle stirring of the cells followed by ammonium sulphate precipitation, ion-exchange and gel chromatography. The native molecule had a Mr in excess of 10⁶ kDa and was made up of subunits with an Mr of 43 kDa. Antisera raised to the adhesin and its subunits reacted with antigens on the surface of B. gingivalis cells. No reaction with fimbriae was seen. The IgG fractions from these antisera inhibited the adherence of B. gingivalis to host tissue. Proteolytic enzymes destroyed binding capability of whole cells and of the purified adhesin but the molecular weight of the haemagglutinin was not altered. A genomic library of B. gingivalis DNA was created in E. coli JM83. 5500 colonies were screened by a colony immunoassay with anti-S. gingivalis serum and by a direct haemagglutinating assay. 337 clones tested positive by the immunoassay and two clones, 1-3,and 1-49 tested positive for haemagglutinating activity. Both haemagglutinating positive recombinants had inserts of 3.2 kb. One clone, 1-49 was chosen for further characterization. E. coli 1-49 expressed a protein of 43 kDa that was not present in E. coli JM 83 control as seen by SDS-PAGE and Western blot analysis. Anti-1-49 serum inhibited the haemagglutinating activity of B. gingivalis and E. coli 1-49. This serum reacted with surface molecules on B. gingivalis and E. coli 1-49 as seen by immunogold electron microscopy and immunofluorescence, and to the purified haemagglutinin by Western blot analysis. Like the haemagglutinin on B. gingivalis, the haemagglutinating activity of E. coli 1-49 was destroyed by heating and proteolytic enzymes but the apparent size of the molecule as determined by SDS-PAGE was not affected. A bacterial coaggregating adhesin from B. gingivalis was isolated and characterized. The isolation procedure involved adsorption of the solubilized adhesin on S. mitis followed by elution with glycine buffer. SDS-PAGE of the boiled adhesin revealed a protein with an Mr of 46 kDa. Proteolytic digestion destroyed all bacterial aggregating activity and hydrolysed the 46 kd protein. Antisera raised to the 46 kDa protein reacted with surface molecules on all strains of B. gingivalis tested. This antiserum inhibited the coaggregation reaction between B. gingivalis and other bacteria. Vesicles produced by B. gingivalis were found to enhance the binding of S. sanguis to serum coated hydroxy apatite (SeHA). Maximum vesicle mediated binding took place at 37°C and was destroyed by heating. The lipopolysaccharide from several black pigmented bacteroides were isolated and characterized physically, chemically and immunologically. All of the LPS were of the smooth type and contained the sugars rhamnose, glucose, galactose, glucosamine and galactosamine; no KDO or heptose were found.
Science, Faculty of
Microbiology and Immunology, Department of
Graduate

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10

Xie, Hua. "Regulation of fimbrillin expression in Porphyromonas gingivalis". Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/6392.

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Più fonti

Libri sul tema "Gingivalis"

1

Goulbourne, P. Andrew. Evidence for the role of fimbriae in the adhesion of bacteroides gingivalis to actinomyces viscosus. Ottawa: National Library of Canada, 1990.

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2

Loomer, Peter Michael. The direct effects of Porphyromonas Gingivalis 2561 on bone formation and mineral resorption in vitro. [Toronto: University of Toronto, Faculty of Dentistry], 1997.

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3

Sun, Frank. Identification of Porphyromonas (Bacteroides) Gingivalis outer membrane proteins that bind to and degrade human matrix proteins. [Toronto: Faculty of Dentistry, University of Toronto, 1992.

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4

Gingival. Palencia, España: Menoscuarto Ediciones, 2012.

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5

Kasaj, Adrian, a cura di. Gingival Recession Management. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-70719-8.

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6

Ruiz, Jose-Luis. Supra-Gingival Minimally Invasive Dentistry. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781118976449.

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7

Chou, Debra Hsin-I. TNF-r̀egulation of phagocytosis in human gingival fibroblasts. Ottawa: National Library of Canada, 1995.

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Chou, Debra Hsin-I. TNF-[alpha] regulation of phagocytosis in human gingival fibroblasts. [Toronto: Faculty of Dentistry, University of Toronto], 1995.

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9

Issa, Roger. The effect of benzydamine HCL on human plaque and gingival tissues. [Toronto]: Faculty of Dentistry, University of Toronto, 1986.

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10

Andlin-Sobocki, Anna. Gingival recession, keratinized and attached gingiva in anterior teeth of children. Umeå: [University of Umeå], 1993.

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Capitoli di libri sul tema "Gingivalis"

1

Genco, Caroline Attardo, Waltena Simpson e Teresa Olczak. "Porphyromonas gingivalis". In Iron Transport in Bacteria, 329–43. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816544.ch21.

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2

Ringelmann, R., e Beate Heym. "Entamoeba gingivalis". In Parasiten des Menschen, 136. Heidelberg: Steinkopff, 1991. http://dx.doi.org/10.1007/978-3-642-85397-5_39.

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3

Mehlhorn, Heinz. "Entamoeba gingivalis". In Encyclopedia of Parasitology, 931–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_3843.

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4

Mehlhorn, Heinz. "Entamoeba gingivalis". In Encyclopedia of Parasitology, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_3843-1.

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5

Takeuchi, Hiroki, e Atsuo Amano. "Invasion of Gingival Epithelial Cells by Porphyromonas gingivalis". In Periodontal Pathogens, 215–24. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0939-2_21.

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6

Arndt, Annette, e Mary Ellen Davey. "Porphyromonas gingivalis: surface polysaccharides as virulence determinants". In Interface Oral Health Science 2009, 382–87. Tokyo: Springer Japan, 2010. http://dx.doi.org/10.1007/978-4-431-99644-6_111.

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7

Yongqing, Tang, Jan Potempa, Robert N. Pike e Lakshmi C. Wijeyewickrema. "The Lysine-Specific Gingipain of Porphyromonas gingivalis". In Advances in Experimental Medicine and Biology, 15–29. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-8414-2_2.

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8

Amano, Atsuo, Youn-Hee Choi e Hiroki Takeuchi. "Genotyping of Porphyromonas gingivalis in Relationship to Virulence". In Periodontal Pathogens, 53–59. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0939-2_6.

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9

Hasegawa, Yoshiaki, Keiji Nagano, Yukitaka Murakami e Richard J. Lamont. "Purification of Native Mfa1 Fimbriae from Porphyromonas gingivalis". In Periodontal Pathogens, 75–86. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0939-2_8.

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10

Heidler, Thomas, e Karina Persson. "Crystallization of Recombinant Fimbrial Proteins of Porphyromonas gingivalis". In Periodontal Pathogens, 87–96. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0939-2_9.

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Atti di convegni sul tema "Gingivalis"

1

De la Garza-Ramos, M. A., A. Alcázar-Pizaña, M. Garza-Enriquez, R. Caffesse, V. Aguirre-Arzola, L. J. Galán-Wong e B. Pereyra-Alférez. "Streptococcus intermedius trigger quorum-sensing genes in Porphyromonas gingivalis". In Proceedings of the III International Conference on Environmental, Industrial and Applied Microbiology (BioMicroWorld2009). WORLD SCIENTIFIC, 2010. http://dx.doi.org/10.1142/9789814322119_0113.

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2

Harris, David M. "Laser antisepsis of Phorphyromonas gingivalis in vitro with dental lasers". In Biomedical Optics 2004, a cura di Peter Rechmann, Daniel Fried e Thomas Hennig. SPIE, 2004. http://dx.doi.org/10.1117/12.549028.

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3

Sieron, Aleksander, Andrzej Wiczkowski, Mariusz Adamek, Lucja Dyla, Sebastian Mazur e Beata Wierucka-Mlynarczyk. "Photodynamic destruction of Porphyromonas gingivalis induced by delta-aminolaevulinic acid". In SPIE Proceedings, a cura di Leonardo Longo, Alfons G. Hofstetter, Mihail-Lucian Pascu e Wilhelm R. A. Waidelich. SPIE, 2004. http://dx.doi.org/10.1117/12.584427.

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4

Mahasneh, Arwa M., Michele Darby, Lynn Tolle, Mounir Laroussi e Wayne Hynes. "Bactericidal effects of low temperature atmospheric pressure plasma on Porphyromonas gingivalis". In 2010 IEEE 37th International Conference on Plasma Sciences (ICOPS). IEEE, 2010. http://dx.doi.org/10.1109/plasma.2010.5534217.

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5

Villarreal-Garcίa, L. E., A. Oranday-Cárdenas, M. A. de la Garza-Ramos, C. Rivas-Morales, M. J. Verde-Star e J. A. Gόmez-Treviño J. Alberto. "Activity methanolic extracts of Azadirachta indica (A. Juss) on P. gingivalis". In MICROBES IN APPLIED RESEARCH - Current Advances and Challenges. WORLD SCIENTIFIC, 2012. http://dx.doi.org/10.1142/9789814405041_0092.

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6

Jan, Ming-Shiou, Wan-Ting Chen, Yu-Jen Chen, Chia-Wei Lin, Wen-Wei Chang, Chung-Hung Tsai, Jia-Shiou Peng e Li-Jin Hsu. "Abstract 235: Probiotics amelioratePorphyromonas gingivalis-promoted pancreatic cancer progression in oncogenicKrastransgenic mice". In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-235.

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7

Mechid, Farida, Houda Hafirassou, Malika Meddad, Samir Salah, Saida Merad, Nawel Blidi e Chafia Makhloufi-Dahou. "AB0255 CLINICO- BIOLOGICAL PROFILE OF RHEUMATOID ARTHRITIS WITH PERIODONTITIS AND PORPHYROMONAS GINGIVALIS". In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3342.

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8

Jenning, M., B. Marklein, Z. Konthur, U. Nonhoff, G.-R. Burmester e K. Skriner. "P043 Infection with citrullinating porphyromonas gingivalis can induce autoimmunity to human ribosomal proteins". In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.35.

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9

Wang, Zhi, Xi Wang e Yiqun Jia. "Abstract 2358: Porphyromonas gingivalis promotes colorectal cancer development by regulating NLRP3 inflammasome signaling". In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2358.

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10

De La Garza-Ramos, M. A., A. L. Luna-Ayala, M. Garza-Enriquez, D. S. Martinez-Carreon, B. Pereyra-Alférez e R. G. Caffesse. "Streptococcus intermedius can module the expression of some virulence factors in Porphyromonas gingivalis". In MICROBES IN APPLIED RESEARCH - Current Advances and Challenges. WORLD SCIENTIFIC, 2012. http://dx.doi.org/10.1142/9789814405041_0116.

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Rapporti di organizzazioni sul tema "Gingivalis"

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J.P, Babu. Long-term dental adhesive toxicity on human gingival fibroblasts and epithelial cells. Science Repository, giugno 2019. http://dx.doi.org/10.31487/j.dobcr.2019.03.01.

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2

Moraschini, Vittorio, Monica Calasans-Maia, Jamil Shibli e Suelen Sartoretto. Effectiveness of autogenous graft substitutes for gingival phenotype modification on dental implants: a network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, ottobre 2020. http://dx.doi.org/10.37766/inplasy2020.10.0056.

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3

Moraschini, Vittorio, Monica Calasans-Maia, Alexandra Dias, Márcio Formiga, Suelen Sartoretto e Jamil Shibli. Effectiveness of connective tissue graft substitutes for the treatment of gingival recessions using coronally advanced flap: a network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, giugno 2020. http://dx.doi.org/10.37766/inplasy2020.6.0075.

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4

Bolyarova, Theodora, Raya Grozdanova, Gergana Micheva, Maria Dencheva e Tsvetelina Velikova. Effect of Diode Laser Treatment on the Level of IL‑6 in the Gingival Crevicular Fluid in Patients with Chronic Periodontitis. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, febbraio 2019. http://dx.doi.org/10.7546/crabs.2019.01.17.

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5

Meza-Mauricio, Jonathan, Camila Furquim, Willy Bustillos, David Soto-Peñaloza, David Peñarrocha-Oltra, Belen Retamal-Valdes e Marcelo Faveri. Does enamel matrix derivate application provide additional clinical benefits in the treatment of upper gingival recessions Class I and II of Miller? A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, ottobre 2020. http://dx.doi.org/10.37766/inplasy2020.10.0048.

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Meza-Mauricio, Jonathan, Camila Pinheiro Furquim, Antonella Geldres, Gerardo Mendoza-Azpur, Belen Retamal-Valdes e Marcelo Faveri. Is the use of platelet rich fibrin effective in the healing, pain and control of post-operative bleeding of palatine area after harvesting free gingival graft? A systematic review of randomized clinical studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, gennaio 2021. http://dx.doi.org/10.37766/inplasy2021.1.0037.

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7

Meza-Mauricio, Jonathan, Camila Pinheiro Furquim, Antonella Geldres, Gerardo Mendoza- Azpur, Belen Retamal-Valdes, Vittorio Moraschini e Marcelo Faveri. Is the use of platelet rich fibrin effective in the healing, pain and control of post-operative bleeding of palatine area after harvesting free gingival graft? A systematic review of randomized clinical studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, gennaio 2021. http://dx.doi.org/10.37766/inplasy2021.1.0113.

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