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Добірка наукової літератури з теми "Denticola"

Автор: Grafiati

Опубліковано: 3 червня 2025

Оновлено: 31 липня 2025

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Статті в журналах з теми "Denticola"

1

Brissette, Catherine A., та Sheila A. Lukehart. "Mechanisms of Decreased Susceptibility to β-Defensins by Treponema denticola". Infection and Immunity 75, № 5 (2007): 2307–15. http://dx.doi.org/10.1128/iai.01718-06.

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ABSTRACT Treponema denticola, a periodontal pathogen, is relatively resistant to human beta-defensins, which are small cationic antimicrobial peptides produced by a number of cells, including the gingival epithelium. Using two independent methods, we previously demonstrated that T. denticola proteases are not responsible for decreased vulnerability to defensins. In this study, we confirmed that the major outer membrane protease, dentilisin, is not responsible for T. denticola insensitivity to defensins and examined several other possible mechanisms, including reduced binding to the bacterial s

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2

Kurniyati, Kurni, and Chunhao Li. "pyrFas a Counterselectable Marker for Unmarked Genetic Manipulations in Treponema denticola." Applied and Environmental Microbiology 82, no. 4 (2015): 1346–52. http://dx.doi.org/10.1128/aem.03704-15.

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ABSTRACTThe pathophysiology ofTreponema denticola, an oral pathogen associated with both periodontal and endodontic infections, is poorly understood due to its fastidious growth and recalcitrance to genetic manipulations. Counterselectable markers are instrumental in constructing clean and unmarked mutations in bacteria. Here, we demonstrate thatpyrF, a gene encoding orotidine-5′-monophosphate decarboxylase, can be used as a counterselectable marker inT. denticolato construct marker-free mutants.T. denticolais susceptible to 5-fluoroorotic acid (5-FOA). To establish apyrF-based counterselectab

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3

Yang, Po Fong, Meja Song, David A. Grove, and Richard P. Ellen. "Filamentous Actin Disruption and Diminished Inositol Phosphate Response in Gingival Fibroblasts Caused byTreponema denticola." Infection and Immunity 66, no. 2 (1998): 696–702. http://dx.doi.org/10.1128/iai.66.2.696-702.1998.

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ABSTRACT Previous reports have shown that Treponema denticolacauses rearrangement of filamentous actin (F-actin) in human gingival fibroblasts (HGF). The purpose of this investigation was to determine the effect of T. denticola on the generation of inositol phosphates (IPs) in relation to a time course for F-actin disruption in HGF. Cultured HGF were exposed to washed cells of T. denticola ATCC 35405 for 140 min. Changes in the fluorescence intensity of rhodamine-phalloidin-labeled F-actin in serial optical sections of single HGF were quantified by confocal microscopy image analysis. The perce

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4

Battikhi, Tulin, Wilson Lee, Christopher A. G. McCulloch, and Richard P. Ellen. "Treponema denticola Outer Membrane Enhances the Phagocytosis of Collagen-Coated Beads by Gingival Fibroblasts." Infection and Immunity 67, no. 3 (1999): 1220–26. http://dx.doi.org/10.1128/iai.67.3.1220-1226.1999.

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ABSTRACT Human gingival fibroblasts (HGFs) degrade collagen fibrils in physiological processes by phagocytosis. Since Treponema denticola outer membrane (OM) extract perturbs actin filaments, important structures in phagocytosis, we determined whether the OM affects collagen phagocytosis in vitro by HGFs. Phagocytosis was measured by flow cytometric assessment of internalized collagen-coated fluorescent latex beads. Confluent HGFs pretreated with T. denticola ATCC 35405 OM exhibited an increase in the percentage of collagen phagocytic cells (phagocytosis index [PI]) and in the number of beads

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5

Idrus, Erik, Willy Hartanto, Widya Lestari, and Dewi Fatma Suniarti. "The role of Treponema denticola in the periodontitis alveolar bone damage: Systematic review." Odonto : Dental Journal 10, no. 2 (2023): 314. http://dx.doi.org/10.30659/odj.10.2.314-325.

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Background: Periodontitis is a chronic inflammation condition of the periodontal tissue, which causes irreversible, progressive deterioration of the tooth-supporting tissue, leading to tooth loss. One of the main bacteria in the pathogenesis of periodontitis is Treponema denticola. Its involvement in periodontitis includes producing and releasing various virulence factors that further modulate inflammation and ignite alveolar bone destruction. Objective: To examine Treponema denticola's role in the mechanism of alveolar bone damage in periodontitis. Method: This systematic review was conducted

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6

Brissette, Catherine A., та Sheila A. Lukehart. "Treponema denticola Is Resistant to Human β-Defensins". Infection and Immunity 70, № 7 (2002): 3982–84. http://dx.doi.org/10.1128/iai.70.7.3982-3984.2002.

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ABSTRACT Spirochetes, including Treponema denticola, are implicated in the pathogenesis of periodontal disease. Because T. denticola lacks lipopolysaccharides that serve as targets for human β-defensin (hβD) binding, we postulated that T. denticola would resist killing by hβD. We showed that T. denticola is resistant to hβD-1 and -2. Protease inhibitors did not enhance killing of T. denticola by hβD-2, suggesting that degradation of hβD-2 by treponemal proteases is not a major factor in T. denticola resistance.

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Chi, Bo, Ronald J. Limberger, and Howard K. Kuramitsu. "Complementation of a Treponema denticola flgE Mutant with a Novel Coumermycin A1-Resistant T. denticola Shuttle Vector System." Infection and Immunity 70, no. 4 (2002): 2233–37. http://dx.doi.org/10.1128/iai.70.4.2233-2237.2002.

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ABSTRACT By using the mutated gyrB gene from a spontaneous coumermycin A1-resistant Treponema denticola, an Escherichia coli-T. denticola shuttle vector that renders T. denticola resistant to coumermycin was constructed. The complete T. denticola flgE gene was cloned into the shuttle vector pKMCou, and the vector was transformed into the T. denticola ATCC 33520 flgE erythromycin-resistant knockout mutant HL210. The coumermycin-resistant transformants were motile and restored FlgE activity. This complementation system should prove useful in studying the virulence factors of T. denticola and unc

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8

Vesey, Peter M., and Howard K. Kuramitsu. "Genetic analysis of Treponema denticola ATCC 35405 biofilm formation." Microbiology 150, no. 7 (2004): 2401–7. http://dx.doi.org/10.1099/mic.0.26816-0.

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Анотація:

Treponema denticola is a major aetiological organism implicated in periodontal disease. The interaction of T. denticola with other oral bacteria, in particular Porphyromonas gingivalis, in biofilm formation is thought to be an important step in the onset of periodontal disease. The interaction between T. denticola and P. gingivalis has been examined using a panel of T. denticola mutants and their effects on mixed biofilm formation tested in a static biofilm model. T. denticola ATCC 35405 did not form detectable biofilms on various inert surfaces. However, the spirochaete was demonstrated to fo

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9

Wu, Linrui, Xinyi Su, Zhiqun Tang та ін. "Treponema denticola Induces Neuronal Apoptosis by Promoting Amyloid-β Accumulation in Mice". Pathogens 11, № 10 (2022): 1150. http://dx.doi.org/10.3390/pathogens11101150.

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Background: Neuronal apoptosis is a major contributor to Alzheimer’s disease (AD). Periodontitis is a significant risk factor for AD. The periodontal pathogens Porphyromonas gingivalis and Treponema denticola have been shown to initiate the hallmark pathologies and behavioral symptoms of AD. Studies have found that T. denticola infection induced Tau hyperphosphorylation and amyloid β accumulation in the hippocampi of mice. Aβ accumulation is closely associated with neuronal apoptosis. However, the roles of T. denticola in neuronal apoptosis remain unclear and its roles in AD pathology need fur

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10

Shin, Ji Eun, Young Sook Kim, Ju-Eun Oh, Byung-Moo Min та Youngnim Choi. "Treponema denticola Suppresses Expression of Human β-Defensin-3 in Gingival Epithelial Cells through Inhibition of the Toll-Like Receptor 2 Axis". Infection and Immunity 78, № 2 (2009): 672–79. http://dx.doi.org/10.1128/iai.00808-09.

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ABSTRACT We reported previously that Treponema denticola, one of the periodontal pathogens, suppresses the expression of human β-defensins (HBDs) in human gingival epithelial cells. To identify the mechanisms involved in this suppression, immortalized and normal human gingival epithelial cells were infected with live or heat-killed T. denticola for 24 h, and then the expression of HBDs was examined by real-time RT-PCR. Live T. denticola suppressed the expression of HBD-3 substantially and also suppressed the expression of HBD-1 and HBD-2. However, heat-killed bacteria did not produce a suppres

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Дисертації з теми "Denticola"

1

Bamford, Caroline V. "Treponema denticola interactions with host proteins." Thesis, University of Bristol, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434742.

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2

Bouchard, Dominique. "Caractérisation biochimique de l'intégrase de l'intégron de Treponema denticola." Thesis, Université Laval, 2006. http://www.theses.ulaval.ca/2006/23650/23650.pdf.

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3

Miller, Daniel Patrick. "CHARACTERIZATION OF COMPLEMENT EVASION OF THE PERIOPATHOGEN, TREPONEMA DENTICOLA." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3478.

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Periodontitis is a polymicrobially-induced, chronic inflammatory disease of the tissues that support and surround the tooth. While greater than 500 organisms are found in dental plaque, Treponema denticola is one of only a few species associated with disease. It has been hypothesized that oral bacteria disrupt host homeostasis through manipulation of the innate immune system. In this study, we examine the impact of binding and subsequent cleavage of factor H, a complement regulator, by T. denticola in the evasion and subversion of complement. The molecular interaction between the sole FH-bindi

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4

Patel, Dhara T. "ASSESSMENT OF A PREDICTED DIGUANYLATE CYCLASE IN TREPONEMA DENTICOLA." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5591.

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Periodontal disease is a progressive inflammatory condition that is characterized by the reabsorption of alveolar bone, the destruction of connective tissue, and edentulism. It is caused by a dysbiosis in the oral microbiome as a result of a shift from a Gram-positive aerobic bacterial population, to one that becomes more Gram-negative and anaerobic. Treponema denticola is thought to drive this diseased state based on its role as a keystone periopathogen. A major component of T.denticola’s invasiveness is its motility, which allows the spirochete to penetrate and disseminate through tissues. T

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5

Leung, Wai Keung. "Effects of Treponema denticola on an oral epithelial cell model." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape17/PQDD_0009/NQ34575.pdf.

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6

Tegels, Brittney. "Analysis of plasminogen binding to Treponema denticola, a key periopathogen." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/556.

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Periodontitis is a chronic inflammatory disease that affects over 116 million adults in the United States. A shift in the normal microflora occurs as periodontal disease develops resulting in a larger number of Gram-negative anaerobes and spirochetes. An increase in the oral spirochete, Treponema denticola, is highly correlated with periodontal disease progression and severity. The ability of this periopathogen to thrive in the subgingival crevice is dependent on complement evasion mechanisms. Earlier analyses demonstrated that the primary mechanism of T. denticola serum resistance is bind

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7

Brissette, Catherine Ayn. "Interactions of oral spirochetes with the innate immune mechanisms of the gingival epithelium /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/9289.

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8

Juni, Sarkar. "Characterization of Hpk2-Rrp2, two-component regulatory system in Treponema denticola." VCU Scholars Compass, 2011. http://scholarscompass.vcu.edu/etd/268.

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Treponema denticola levels in the gingival crevice become elevated as periodontal disease develops. Oral treponemes may account for as much as 40% of the total bacterial population in the periodontal pocket. The stimuli that trigger enhanced growth of T. denticola and the mechanisms associated with the transmission of these signals remain to be defined. A hypothesis was set that the T. denticola ORFs tde1970 (histidine kinase) and tde1969 (response regulator) constitute a functional two component regulatory system that regulates, at least in part, responses to the changing environmental condi

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9

Haus, Karin. "Charakterisierung eines Flagellin-Genclusters aus Treponema maltophilum." Tönning Lübeck Marburg Der Andere Verl, 2008. http://d-nb.info/991846397/04.

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10

Gaibani, Paolo <1980&gt. "Role of treponema denticola in the pathogenesis and progression of Periodontal Disease." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2010. http://amsdottorato.unibo.it/2284/1/Paolo_Gaibani.pdf.

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Книги з теми "Denticola"

1

Filippo, Anna Beatriz De. Cytopathic effects of Treponema denticola on KB epithelial cells. s.n.], 1993.

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2

Ivic, Ana. Molecular characterization and detection of the periodontal spirochaete "Treponema denticola". University of Birmingham, 1991.

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3

Yang, Po Fong. Filamentous actin disruption and diminished inositol phosphate response in gingival fibroblasts caused by Treponema denticola. University of Toronto, Faculty of Dentistry], 1998.

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4

Battikhi, Tulin. Treponema Denticola outer membrane extract enhances the phagocytosis of collagen coated-beads by human gingival fibroblasts. University of Toronto, Faculty of Dentistry], 1998.

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5

Thomas, Bina Agnes Puthengady. Effect of Treponema denticola major outer sheath protein on neutrophil functions in vitro. 2006.

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6

Silva, Andre Paes Batista da. Treponema denticola outer sheath protein (Msp) inhibits the binding step of collagen phagocytosis in fibroblasts. 2003.

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7

Galimanas, Vaia Bailey. Expression of the Treponema denticola dentilisin gene (prtP) and upstream genes in biofilm and planktonic cells under peptide-limiting conditions. 2005.

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8

Le denticulé, cet inconnu: Les assemblages lithiques à denticulés du Paléolithique moyen en Europe. John and Erica Hedges Ltd., 2008.

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9

BLAKESLEE, Thomas. Denticorn Funny Dentist Gift for Unicorn Dental Assistant: Notebook, Notebook Journal Beautiful , Simple, Impressive,size 6x9 Inches, 114 Paperback Pages. Independently Published, 2021.

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Частини книг з теми "Denticola"

1

Kurniyati, Kurni, and Chunhao Li. "Genetic Manipulations of Oral Spirochete Treponema denticola." In Periodontal Pathogens. Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0939-2_2.

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2

Kikuchi, Yuichiro, and Kazuyuki Ishihara. "Characterization of the Treponema denticola Virulence Factor Dentilisin." In Periodontal Pathogens. Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0939-2_17.

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3

Marconi, Richard T. "Gene Regulation, Two Component Regulatory Systems, and Adaptive Responses in Treponema Denticola." In Current Topics in Microbiology and Immunology. Springer International Publishing, 2017. http://dx.doi.org/10.1007/82_2017_66.

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4

McDowell, John V., Daniel P. Miller, Katherine L. Mallory, and Richard T. Marconi. "Treponema denticola: FhbB, Dentilisin, Complement Evasion and the Paradox of Factor H Cleavage." In The Pathogenic Spirochetes: strategies for evasion of host immunity and persistence. Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-5404-5_3.

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Marconi, Richard T. "Erratum to: Gene Regulation, Two Component Regulatory Systems, and Adaptive Responses in Treponema Denticola." In Current Topics in Microbiology and Immunology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/82_2018_95.

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6

"Denticle." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics. Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_4298.

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7

Singhrao, Sim K., Alice Harding, Tal Simmons, Sarita Robinson, Lakshmyya Kesavalu, and StJohn Crean. "Oral Inflammation, Tooth Loss, Risk Factors, and Association with Progression of Alzheimer’s Disease." In Advances in Alzheimer’s Disease. IOS Press, 2022. http://dx.doi.org/10.3233/aiad220038.

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Анотація:

Periodontitis is a polymicrobial chronic inflammatory disease of tooth-supporting tissues with bacterial etiology affecting all age groups, becoming chronic in a subgroup of older individuals. Periodontal pathogens Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola are implicated in the development of a number of inflammatory pathologies at remote organ sites, including Alzheimer’s disease (AD). The initial inflammatory hypothesis proposed that AD hallmark proteins were the main contributors of central nervous system (CNS) inflammation. This hypothesis is expanding to incl

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8

Poole Sophie, Singhrao Sim K., Kesavalu Lakshmyya, Curtis Michael A., and Crean StJohn. "Determining the Presence of Periodontopathic Virulence Factors in Short-Term Postmortem Alzheimer's Disease Brain Tissue." In Advances in Alzheimer’s Disease. IOS Press, 2017. https://doi.org/10.3233/978-1-61499-706-1-105.

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The aim of this study was to establish a link between periodontal disease and Alzheimer's disease (AD) with a view to identifying the major periodontal disease bacteria (Treponema denticola, Tannerella forsythia, and Porphyromonas gingivalis) and/or bacterial components in brain tissue from 12h postmortem delay. Our request matched 10 AD cases for tissue from Brains for Dementia Research alongside 10 non-AD age-related controls with similar or greater postmortem interval. We exposed SVGp12, an astrocyte cell line, to culture supernatant containing lipopolysaccharide (LPS) from the putative per

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Poole Sophie, Singhrao Sim K., Chukkapalli Sasanka, et al. "Active Invasion of Porphyromonas gingivalis and Infection-Induced Complement Activation in ApoE." In Advances in Alzheimer’s Disease. IOS Press, 2017. https://doi.org/10.3233/978-1-61499-706-1-119.

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Periodontal disease is a polymicrobial inflammatory disease that leads to chronic systemic inflammation and direct infiltration of bacteria/bacterial components, which may contribute to the development of Alzheimer's disease. ApoE&minus;/&minus;mice were orally infected (n=12) with Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Fusobacterium nucleatum as mono-and polymicrobial infections. ApoE&minus;/&minus;mice were sacrificed following 12 and 24 weeks of chronic infection. Bacterial genomic DNA was isolated from all brain tissues except for the F. nu

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"denticule, n." In Oxford English Dictionary, 3rd ed. Oxford University Press, 2023. http://dx.doi.org/10.1093/oed/2139900219.

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Тези доповідей конференцій з теми "Denticola"

1

Kamarajan, Pachiyappan, Islam Ateia, Jae M. Shin, J. Christopher Fenno, and Yvonne L. Kapila. "Abstract 3294: Treponema denticola, a periodontal pathogen, promotes stemness and migration in oral squamous cell carcinoma." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3294.

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2

Prichard, Reid, Wayne Strasser, Chad Cherok, Robert Kacinski, and Amy Lang. "Passive Bristling of Shark Skin Scales at the Micro-Level: A Fundamental Viscous Flow Study to Understand the Separation Control Mechanism." In ASME 2020 Fluids Engineering Division Summer Meeting collocated with the ASME 2020 Heat Transfer Summer Conference and the ASME 2020 18th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/fedsm2020-20457.

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Abstract In this paper, we use a CFD analysis of a simplified, 2D geometry to study the ability of mako shark denticles to mitigate flow separation. We represent the viscous sublayer below a turbulent boundary layer streak as a Couette flow. Incipient separation is simulated by balancing upper wall velocity and adverse pressure gradient to achieve zero net mass flow, and we add various denticle geometries to study their effects. Each modeled denticle protrudes at an angle from 15° to 85° and sublayer blockage ratio from 0.05 to 0.85. Through variation of fluid properties and boundary condition

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3

Bhatia, Dinesh, Devinder Yadav, and Chenggeng Xie. "Aerodynamic drag reduction through sharkskin denticle: an experimental approach." In Seventh International Conference on Electromechanical Control Technology and Transportation (ICECTT 2022), edited by Said Easa. SPIE, 2022. http://dx.doi.org/10.1117/12.2645374.

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4

Bamforth, Tobias, Fang Xia, Ignacio González-Álvarez, Caroline Tiddy, Siyu Hu, and Mark Pearce. "The Preservation of Denticular Dissolution Textures Through Secondary Mineral Overgrowth and Replacement in Intensely Weathered Regolith." In Goldschmidt2022. European Association of Geochemistry, 2022. http://dx.doi.org/10.46427/gold2022.12712.

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Звіти організацій з теми "Denticola"

1

จรัสกุลางกูร, อรวรรณ, กนกวรรณ นิสภกุลธร та รังสินี มหานนท์. การตรวจหาเชื้อแบคทีเรียก่อโรคปริทันต์อักเสบเรื้อรังและเป็นโรคเบาหวานชนิดที่ 2 ที่ควบคุมระดับน้ำตาลในเลือดได้ไม่ดี : รายงานผลการวิจัย. จุฬาลงกรณ์มหาวิทยาลัย, 2009. https://doi.org/10.58837/chula.res.2009.12.

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Анотація:

ผู้ป่วยโรคเบาหวานที่ไม่สามารถควบคุมระดับน้ำตาลในเลือดได้ดี มีความเสี่ยงต่อการสูญเสียระดับการยึดเกาะของอวัยวะปริทันต์และการละลายของกระดูกเบ้าฟันมากขึ้น การเปลี่ยนแปลงสมดุลของเชื้อแบคทีเรียใต้เหงือกอาจเป็นสาเหตุในการเพิ่มความรุนแรงของโรคปริทันต์อักเสบในผู้ป่วยกลุ่มนี้ การวิจัยนี้มีวัตถุประสงค์เพื่อหาความชุกของเชื้อแบคทีเรีย Porphyromonas qingivalis, Tannerella forsythia, Treponema denticola และ Prevotella intermedia ในแผ่นคราบจุลินทรีย์ใต้เหงือกของผู้ป่วยโรคเบาหวานชนิดที่ 2 ที่ควบคุมระดับน้ำตาลในเลือดได้ไม่ดีเปรียบเทียบกับผู้ป่วยที่ไม่เป็นโรคเบาหวาน โดยศึกษาในผู้ป่วยโรคปริทันต์อักเสบเรื้อรังทั่ว

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