TY - JOUR. T1 - Porphyromonas gingivalis Infection Induces Amyloid-β Accumulation in Monocytes/Macrophages. AU - Nie, Ran. AU - Wu, Zhou. AU - Ni, Junjun. AU - Zeng, Fan. AU - Yu, Weixian. AU - Zhang, Yufeng. AU - Kadowaki, Tomoko. AU - Kashiwazaki, Haruhiko. AU - Teeling, Jessica L.. AU - Zhou, Yanmin. PY - 2019/1/1. Y1 - 2019/1/1. N2 - Abnormal accumulation of amyloid-β (Aβ) in the brain is the most significant pathological hallmark of Alzheimers disease (AD). We have found that chronic systemic exposure to lipopolysaccharide of Porphyromonas gingivalis (P. gingivalis) induces the accumulation of Aβ in the brain of middle-aged mice. On the other hand, recent research has shown that circulating Aβ is transferred into the brain; however, the involvement of chronic systemic P. gingivalis infection in the peripheral Aβ metabolism is unknown. We hypothesized that chronic P. gingivalis infection expands Aβ pools in peripheral inflammatory tissues and thereby contributes to the accumulation ...

Periodontitis is a chronic inflammatory disease caused by exaggerated host immune responses to dysregulated microbiota in dental biofilms leading to degradation of tissues and alveolar bone loss. Porphyromonas gingivalis is a major periodontal pathogen and expresses several potent virulence factors. Among these factors, arginine and lysine gingipains are of special importance, both for the bacterial survival/proliferation and the pathological outcome. The major aim of this thesis was to develop and test novel methods for diagnosis and prevention of P. gingivalis infection and periodontitis. In study I, anti-P. gingivalis antibodies were developed in vitro for immunodetection of bacteria in clinical samples using a surface plasmon resonance (SPR)-based biosensor. Specific binding of the antibodies to P. gingivalis was demonstrated in samples of patients with periodontitis and the results were validated using real-time PCR and DNA-DNA checkerboard analysis. In study II, we elucidated the ...

The pathogenicity of the periodontal biofilm is highly dependent on a few key species, of which Porphyromonas gingivalis is considered to be one of the most important pathogens. P. gingivalis expresses a broad range of virulence factors, of these cysteine proteases (gingipains) are of special importance both for the bacterial survival/proliferation and for the pathological outcome. Several cell types, for example, epithelial cells, endothelial cells, dendritic cells, osteoblasts, and fibroblasts, reside in the periodontium and are part of the innate host response, as well as platelets, neutrophils, lymphocytes, and monocytes/macrophages. These cells recognize and respond to P. gingivalis and its components through pattern recognition receptors (PRRs), for example, Toll-like receptors and protease-activated receptors. Ligation of PRRs induces downstream-signaling pathways modifying the activity of transcription factors that regulates the expression of genes linked to inflammation. This is followed by the

Yes. Theres a lot of discussion about it. So, first of all, its a risk factor. So, often, when you see p. gingivalis, or when you see periodontitis, you often see, also, other diseases like diabetes. So, but, they showed the association. But the problem is: both diseases; or a lot of diseases, like cardiovascular diseases; are so complex and caused by different factors, thats its very difficult to find 1 cause or 1 relation. So, there has never been a causal relationship that has been demonstrated. So, what I can say is, maybe, if you have periodontitis with p. gingivalis, there are studies that demonstrate, so: the invasiveness of p. gingivalis. It can go to the liver, and there it can interact with the process of the glucose mechanism. So, the invasiveness, first of all: p. gingivalis makes that it may ... yes, I would say: induce the diabetes. But, on the other hand; you see, for diabetes patients, the problem is there: they may have a loss in bone density. And when you see to the ...

Principal Investigator：TSUKUBA Tomoko, Project Period (FY)：2004 - 2005, Research Category：Grant-in-Aid for Scientific Research (C), Section：一般, Research Field：Functional basic dentistry

Researchers at the University at Buffalo have been able to identify two key components in saliva that could be used to predict the amount of oral bone loss in future.

Background: It has been suggested that bacterial infections have a role in the pathogenesis of rheumatoid arthritis (RA). P gingivalis, a Gram-negative, anaerobic rod, is one of the major pathogens associated with periodontal disease.. Objective: To examine P gingivalis infection and its effects on cell cycle progression and apoptosis of human articular chondrocytes.. Methods: Primary human chondrocytes cultured in monolayers were challenged with P gingivalis. Infection and invasion of P gingivalis into chondrocytes was analysed by scanning electron microscopy, double immunofluorescence and by antibiotic protection and invasion assay. Cell cycle progression of infected chondrocytes was evaluated by flow cytometry. Also, cell apoptosis was visualised by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) of DNA strand breaks and by western blot analysis.. Results: Data showed that P gingivalis could adhere and infect primary human chondrocytes. After chondrocyte ...

K-antigen capsule is one of the key virulence factors of the oral pathogen Porphyromonas gingivalis. This cell surface structure is synthesized by proteins encoded by a series of genes in an operon that is transcribed as a large polycistronic message. Previously, a 77-bp inverted repeat region was identified upstream of the start codon of PG0106, the first gene in the synthesis cluster, and this inverted repeat was predicted to form a large stem-loop structure. Furthermore, two genes that flank the synthesis cluster (PG0104 and PG0121) were also found to be co-transcribed with the K-antigen capsule synthesis operon. Interestingly, these genes are both predicted to encode DNA binding proteins; indicated by their high similarity to other known DNA binding proteins. PG0104 shares a 57% sequence similarity to DNA topoisomerase III from Bacillus subtilis, while PG0121 is 72% similar to DNA binding protein HU of Bacillus caldotenax. The transcript levels of the K-antigen capsule synthesis genes in ...

K-antigen capsule is one of the key virulence factors of the oral pathogen Porphyromonas gingivalis. This cell surface structure is synthesized by proteins encoded by a series of genes in an operon that is transcribed as a large polycistronic message. Previously, a 77-bp inverted repeat region was identified upstream of the start codon of PG0106, the first gene in the synthesis cluster, and this inverted repeat was predicted to form a large stem-loop structure. Furthermore, two genes that flank the synthesis cluster (PG0104 and PG0121) were also found to be co-transcribed with the K-antigen capsule synthesis operon. Interestingly, these genes are both predicted to encode DNA binding proteins; indicated by their high similarity to other known DNA binding proteins. PG0104 shares a 57% sequence similarity to DNA topoisomerase III from Bacillus subtilis, while PG0121 is 72% similar to DNA binding protein HU of Bacillus caldotenax. The transcript levels of the K-antigen capsule synthesis genes in ...

Methods: in vivo laboratory, experimental research was conducted using posttest only control group design. The samples were 20 male Wistar rats divided into 4 groups. Groups I and II were groups injected using LPS P. gingivalis for 6 w and were decapited on the day 3 and day 7, groups III and IV were the control groups (not injected using LPS P. gingivalis) and decapited on the day 3 and day 7. Subsequently, conducting tissue preparation, staining using haematoxilin eosin, and calculating the number of osteoclasts and osteoblasts cells using a microscope (Optilab) with 400x magnification. The results of osteoblast and osteoclast cell calculation were analyzed using ANOVA and LSD one-way test. ...

Atherosclerotic vascular disease is a leading cause of myocardial infarction and cerebrovascular accident, and independent associations with periodontal disease (PD) are reported. PD is caused by polymicrobial infections and aggressive immune responses. Genomic DNA of Porphyromonas gingivalis, the best-studied bacterial pathogen associated with severe PD, is detected within atherosclerotic plaque. We examined causal relationships between chronic P. gingivalis oral infection, PD, and atherosclerosis in hyperlipidemic ApoEnull mice. ApoEnull mice (n = 24) were orally infected with P. gingivalis for 12 and 24 weeks. PD was assessed by standard clinical measurements while the aorta was examined for atherosclerotic lesions and inflammatory markers by array. Systemic inflammatory markers serum amyloid A, nitric oxide, and oxidized low-density lipoprotein were analyzed. P. gingivalis infection elicited specific antibodies and alveolar bone loss. Fluorescent in situ hybridization detected viable P. gingivalis

Porphyromonas gingivalis ATCC ® BAA-308D-5™ Designation: Genomic DNA from Porphyromonas gingivalis strain W83 TypeStrain=False Application:

Periodontitis is a chronic infectious disease that is highly prevalent worldwide and is characterized by inflammation of the gums, and loss of connective tissue and bone support. The Gram-negative anerobic bacterium Porphyromonas gingivalis is generally accepted as the main etiological agent for chronic periodontitis. The objective of this paper is to elucidate the feasibility of achieving protection against periodontitis though immunization against P. gingivalis. Until now, animal studies have showed no complete protection against P. gingivalis. However, current knowledge about P. gingivalis structures could be applicable for further research to develop a successful licensed vaccine and alternative therapeutic strategies. This review reveals that a multicomponent vaccine against P. gingivalis, which includes structures shared among P. gingivalis serotypes, will be feasible to induce broad and complete protection ...

The suitability of a mouse model for host response in the induction of alveolar bone loss by Porphyromonas gingivalis was explored. The mouths of immunocompetent and severe combined immunodeficient (SCID) mice were infected with P. gingivalis ATCC 53977. P. gingivalis was not isolated from the mouths of these mice before infection, but was present at least 42 days after infection. P. gingivalis-specific IgG was present in sera from the infected, immunocompetent mice at the end of these experiments (42 days). Specific IgG was not present in sham-infected or uninfected immunocompetent mice, nor in any immunodeficient mice. Specific IgM was not present in any sera at 42 days. Infected, immunocompetent mice of two strains showed significant bone loss in comparison to sham-infected or uninfected immunocompetent mice (p | 0.05). Infected SCID mice, which are genetically lacking both B and T lymphocytes, also showed significant bone loss compared with sham-infected or uninfected SCID mice (p | 0.05

Porphyromonas gingivalis is a highly proteolytic organism which metabolizes small peptides and amino acids. Indirect evidence suggests that the proteases produced by this microorganism constitute an important virulence factor. In this study, a gene bank of P. gingivalis W83 DNA was constructed by cloning 0.5- to 20-kb HindIII-cut DNA fragments into Escherichia coli DH5 alpha by using the plasmid vector pUC19. A clone expressing a protease from P. gingivalis was isolated on LB agar containing 1% skim milk. The clone contained a 3.0-kb insert that coded for a protease with an apparent molecular mass of 64 kDa. Sequencing part of the 3.0-kb DNA fragment revealed an open reading frame encoding a protein of 482 amino acids with a molecular mass of 62.5 kDa. Putative promoter and termination elements flanking the open reading frame were identified. The activity expressed in E. coli was extensively characterized by using various substrates and protease inhibitors, and the results suggest that it is ...

Chronic periodontitis is strongly associated with composition of the oral biofilm occupying the gingival crevicular aspect of the tooth and its associated root. Some gram-negative, red complex bacteria instigate periodontal bone loss in patients, principal among these Porphyromonas gingivalis. P. gingivalis is a late colonizer, indicating not only its physical location within the oral biofilm, but also the pathogenic dynamic of the interaction between P. gingivalis and the host innate immunity. Among several other subversive tactics, P. gingivalis has been shown to compel receptors vital to the orchestration of an appropriate immune response to co-associate and consequently signal in a way that directly benefits the pathogen. Upon interaction with human monocytes and murine macrophages, P. gingivalis has been shown to induce TLR2 and CXCR4 to co- associate in lipid rafts via its surface fimbriae. The ensuing crosstalk results in a cAMP dependent, PKA mediated inhibition of NF-KB which in turn leads

ATP-dependent serine protease that mediates the selective degradation of mutant and abnormal proteins as well as certain short-lived regulatory proteins. Required for cellular homeostasis and for survival from DNA damage and developmental changes induced by stress. Degrades polypeptides processively to yield small peptide fragments that are 5 to 10 amino acids long. Binds to DNA in a double-stranded, site-specific manner.

Toll-like receptors (TLRs) are a group of pathogen-associated molecular pattern receptors, which play an important role in in-nate immune signaling in response to microbial infection. It has been demonstrated that TLRs are differentially up regulated in response to microbial infection and chronic inflammatory diseases such as atherosclerosis. Furthermore hyperlipidemic mice deficient in TLR2, TLR4, and MyD88 signaling exhibit diminished inflammatory responses and decreased atherosclerosis. Accumulating evidence has implicated specific infectious agents including the periodontal disease pathogen Porphyromonas gingivalis in the progression of atherosclerosis. Evidence in humans suggesting that periodontal infection predisposes to atherosclerosis is derived from studies demonstrating that the periodontal pathogen P. gingivalis resides in the wall of atherosclerotic vessels and seroepidemiological studies demonstrating an association between pathogen-specific IgG antibodies and atherosclerosis. We ...

Cortexyme, Inc. (Nasdaq: CRTX), a clinical stage biopharmaceutical company pioneering a novel, disease-modifying therapeutic approach to treat what it believes to be a key underlying cause of Alzheimers (AD) and other degenerative diseases, today announced the publication of research further documenting the ability of the pathogen Porphyromonas gingivalis to invade neurons and trigger Alzheimers-like neuropathology.

Outer membrane protein A (OmpA) is a key outer membrane protein found in Gram-negative bacteria that contributes to several crucial processes in bacterial virulence. In Porphyromonas gingivalis, OmpA is predicted as a heterotrimer of OmpA1 and OmpA2 subunits encoded by adjacent genes. Here we describe the role of OmpA and its individual subunits in the interaction of P. gingivalis with oral cells. Using knockout mutagenesis, we show that OmpA2 plays a significant role in biofilm formation and interaction with human epithelial cells. We used protein structure prediction software to identify extracellular loops of OmpA2, and determined these are involved in interactions with epithelial cells as evidenced by inhibition of adherence and invasion of P. gingivalis by synthetic extracellular loop peptides and the ability of the peptides to mediate interaction of latex beads with human cells. In particular, we observe that OmpA2-loop 4 plays an important role in the interaction with host cells. These ...

Periodontal disease is of established aetiology in which polymicrobial synergistic ecology has become dysbiotic under the influence of Porphyromonas gingivalis. Following breakdown of the hosts protective oral tissue barriers, P. gingivalis migrates to developing inflammatory pathologies that associate with Alzheimers disease (AD). Periodontal disease is a risk factor for cardiovascular disorders (CVD), type II diabetes mellitus (T2DM), AD and other chronic diseases, whilst T2DM exacerbates periodontitis. This study analysed the relationship between the P. gingivalis/host interactome and the genes identified in genome-wide association studies (GWAS) for the aforementioned conditions using data from GWASdb (P

Porphyromonas gingivalis porphypain protein: isolated from Prophyromonas gingivalis W12; amino acid sequence in first source; GenBank U42210; do not confuse with PrtP from Lactococcus

Porphyromonas gingivalis KGP-381 protein: gene kgp(381) has high homology with the proteolytic domain of cysteine proteases/hemagglutination genes; MW 40 kDa; amino acid sequence in first source

Characterization of a second cell-associated Arg-specific cysteine proteinase of Porphyromonas gingivalis and identification of an adhesin-binding motif involved in association of the prtR and prtK proteinases and adhesins into large complexes

http://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1932-6203&volume=7&issue=12&spage=e51008&epage=&date=2012&atitle=Baicalin+Downregulates+Porphyromonas+gingivalis+Lipopolysaccharide-Upregulated+IL-6+and+IL-8+Expression+in+Human+Oral+Keratinocytes+by+Negative+Regulation+of+TLR+ ...

Results Intratracheal infection with 5x107 P. gingivalis did not lead to systemic infection and live bacteria were eliminated twenty-four hours postinfection from the lungs. Moreover, no live bacteria were found in other organs and blood at any time after bacterial administration. However, significant ankle swelling occurred in DBA/1 mice 7 days after P. gingivalis challenge. In contrast to DBA/1, BALB/c and C57BL/6 mice were resistant to joint inflammation generated by P. gingivalis intratracheal infection. The arthritic joints in DBA/1 mice exhibited inflammatory changes in synovial tissue. Serum proinflammatory mediators such as IL-6, TNF-alpha, IL-10, MCP-1 were found to be elevated one week after infection, which correlated with the onset of inflammatory changes in the joints.. Other routes of P. gingivalis administration did not lead to inflammatory changes in the joints.. ...

Projekt „Repozytorium otwartego dostępu do dorobku naukowego i dydaktycznego UJ współfinansowany w ramach poddziałania 2.3.1 „Cyfrowe udostępnianie zasobów nauki Programu Operacyjnego Polska Cyfrowa z Europejskiego Funduszu Rozwoju Regionalnego i budżetu państwa na podstawie umowy o dofinansowanie nr POPC.02.03.01-00-0030/17-00 ...

Porphyromonas gingivalis (P.Gingivalis) es un microorganismo comprometido en el inicio y progresión de la enfermedad periodontal crónica y agresiva, y es considerado su principal agente etiológico. Esta bacteria cuenta con una serie defactores de virulencia que le permiten, iniciar el proceso infeccioso, perpetuar la infección y también transformar la placa dental benigna en una comunidad microbiana patógena. Estudiar sus factores de virulencia y su capacidad de modular la respuesta inmunológica del huésped es muy importante para comprender el papel de este patógeno en el desarrollo y establecimiento de la enfermedad. Esta revisión proporciona una visión actual sobre los factores de virulencia y su impacto sobre la respuesta inmunológica en relación con la patogénesis de la enfermedad periodontal. Porphyromonas gingivalis (P. Gingivalis) is a microorganism involved in the onset and progression of chronic and aggressive periodontal disease, and is considered its main etiological ...

p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class=publication>Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href=http://www.nrbook.com/b/bookcpdf.php>Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...

Principal Investigator：田中 雅子, Project Period (FY)：1991, Research Category：Grant-in-Aid for Encouragement of Young Scientists (A), Research Field：Morphological basic dentistry

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Comparison of P. gingivalis HmuY and its homologs from P. intermedia and T. forsythia.Amino acid alignment (A) and approximated protein structures (B). P. inter

It has been demonstrated that the Porphyromonas gingivalis cysteine proteinases (gingipains) activate and/or degrade a broad range of host proteins. Inactivation of gingipains R prior to infection of mice results in a decrease in the virulence of P. gingivalis. Analysis of mouse, rabbit, and chicken antisera raised to gingipain R1 demonstrated that the hemagglutinin domains of gingipains are very immunogenic; however, immunization of mice with a peptide derived from the hemagglutinin domain did not protect mice from P. gingivalis infection. Our recent studies indicate that immunization of mice with a peptide corresponding to the N-terminus of the catalytic domain of gingipains R results in the generation of an immune response that affords protection of mice from P. gingivalis infection. It is postulated that the protection observed results from the inactivation of the enzymatic activity of gingipains R as a result of antibody recognition of a processing site on the gingipain R precursor.. ...

Background: Porphyromonas gingivalis is a gram-negative bacterium that causes destructive chronic periodontitis. In addition, this bacterium is also involved in the development of cardiovascular disease. The aim of this study was to investigate the effects of P. gingivalis infection on gene and protein expression in human aortic smooth muscle cells (AoSMCs) and its relation to cellular function.. Results: AoSMCs were exposed to viable P. gingivalis for 24 h, whereafter confocal fluorescence microscopy was used to study P. gingivalis invasion of AoSMCs. AoSMCs proliferation was evaluated by neutral red assay. Human genome microarray, western blot and ELISA were used to investigate how P. gingivalis changes the gene and protein expression of AoSMCs. We found that viable P. gingivalis invades AoSMCs, disrupts stress fiber structures and significantly increases cell proliferation. Microarray results showed that, a total of 982 genes were identified as differentially expressed with the threshold log2 ...

TY - JOUR. T1 - Porphyromonas gingivalis may multiply and advance within stratified human junctional epithelium in vitro. AU - Papapanou, P. N.. AU - Sandros, J.. AU - Lindberg, K.. AU - Duncan, M. J.. AU - Niederman, R.. AU - Nannmark, U.. PY - 1994. Y1 - 1994. M3 - Article. C2 - 7799218. VL - 29. SP - 374. EP - 375. JO - Journal of Periodontal Research. JF - Journal of Periodontal Research. SN - 0022-3484. IS - 5. ER - ...

TY - JOUR. T1 - The GroEL protein of Porphyromonas gingivalis accelerates tumor growth by enhancing endothelial progenitor cell function and neovascularization. AU - Lin, F. Y.. AU - Huang, C. Y.. AU - Lu, H. Y.. AU - Shih, C. M.. AU - Tsao, N. W.. AU - Shyue, S. K.. AU - Lin, C. Y.. AU - Chang, Y. J.. AU - Tsai, C. S.. AU - Lin, Y. W.. AU - Lin, S. J.. PY - 2015/6/1. Y1 - 2015/6/1. N2 - Porphyromonas gingivalis is a bacterial species that causes destruction of periodontal tissues. Additionally, previous evidence indicates that GroEL from P. gingivalis may possess biological activities involved in systemic inflammation, especially inflammation involved in the progression of periodontal diseases. The literature has established a relationship between periodontal disease and cancer. However, it is unclear whether P. gingivalis GroEL enhances tumor growth. Here, we investigated the effects of P. gingivalis GroEL on neovasculogenesis in C26 carcinoma cell-carrying BALB/c mice and chick eggs in vivo ...

Porphyromonas gingivalis, the major etiologic agent of chronic periodontitis, produces a broad spectrum of virulence factors, including Arg- and Lys-gingipain cysteine proteinases. In this study, we investigated the capacity of P. gingivalis gingipains to trigger a proinflammatory response in human monocyte-derived macrophages. Both Arg- and Lys-gingipain preparations induced the secretion of TNF-α and IL-8 by macrophages. Stimulation of macrophages with Arg-gingipain A/B preparation at the highest concentration was associated with lower amounts of cytokines detected, a phenomenon likely related to proteolytic degradation. The inflammatory response induced by gingipains was not dependent of their catalytic activity since heat-inactivated preparations were still effective. Stimulating macrophages with gingipain preparations was associated with increased levels of phosphorylated p38α MAPK suggesting its involvement in cell activation. In conclusion, our study brought clear evidence that P. gingivalis

TY - JOUR. T1 - Influence of immunization on Porphyromonas gingivalis colonization and invasion in the mouse chamber model. AU - Genco, C. A.. AU - Kapczynski, D. R.. AU - Cutler, C. W.. AU - Arko, R. J.. AU - Arnold, R. R.. N1 - Copyright: Copyright 2020 Elsevier B.V., All rights reserved.. PY - 1992. Y1 - 1992. N2 - The effects of immunization with invasive or noninvasive Porphyromonas (Bacteroides) gingivalis strains on the pathogenesis of infection in a mouse chamber model were examined. BALB/c mice were immunized by a single injection of heat-killed P. gingivalis invasive strain A7436 or W83 or noninvasive strain 33277, HG405, or 381 directly into subcutaneous chambers. P. gingivalis-specific antibody was detected in chamber fluid 21 days postimmunization, and mice were subsequently challenged by injection of exponential-phase P. gingivalis into chambers. Immunization with A7436 or W83 followed by challenge with A7436 protected mice against secondary abscess formation and death; however, P. ...

Porphyromonas gingivalis, a periodontal pathogen, can invade primary cultures of gingival epithelial cells. Optimal invasion occurred at a relatively low multiplicity of infection (i.e., 100) and demonstrated saturation at a higher multiplicity of infection. Following the lag phase, during which bacteria invaded poorly, invasion was independent of growth phase. P. gingivalis was capable of replicating within the epithelial cells. Invasion was an active process requiring both bacterial and epithelial cell energy production. Invasion was sensitive to inhibitors of microfilaments and microtubules, demonstrating that epithelial cell cytoskeletal rearrangements are involved in bacterial entry. P. gingivalis, but not epithelial cell, protein synthesis was necessary for invasion. Invasion within the epithelial cells was not blocked by inhibitors of protein kinase activity. Invasion was inhibited by protease inhibitors, suggesting that P. gingivalis proteases may be involved in the invasion process. ...

TY - JOUR. T1 - Innate immune recognition of invasive bacteria accelerates atherosclerosis in apolipoprotein E-deficient mice. AU - Gibson, Frank C.. AU - Hong, Charlie. AU - Chou, Hsin H.. AU - Yumoto, Hiromichi. AU - Chen, Jiqiu. AU - Lien, Egil. AU - Wong, Jodie. AU - Genco, Caroline Attardo. PY - 2004/6/8. Y1 - 2004/6/8. N2 - Background - Infectious diseases have emerged as potential risk factors for cardiovascular disease (CVD). Epidemiological studies support a connection between periodontal disease, a chronic inflammatory disease of the supporting tissues of the teeth, and CVD. Methods and Results - To directly test the connection between periodontal disease and atherosclerosis, apoE-/- mice were orally challenged with the periodontal disease pathogen Porphyromonas gingivalis or an invasion-impaired P gingivalis fimbriae-deficient mutant (FimA-). Both wild-type P gingivalis and the FimA- mutant were detected in blood and aortic arch tissue of apoE-/- mice by PCR after challenge. ApoE-/- ...

Polyphosphate (polyP) has bactericidal activity against a gram-negative periodontopathogen Porphyromonas gingivalis, a black-pigmented gram-negative anaerobic rod. However, current knowledge about the mode of action of polyP against P. gingivalis is incomplete. To elucidate the mechanisms of antibacterial action of polyP against P. gingivalis, we performed the full-genome gene expression microarrays, and gene ontology (GO) and protein-protein interaction network analysis of differentially expressed genes (DEGs). We successfully identified 349 up-regulated genes and 357 down-regulated genes (|1.5-fold, P | 0.05) in P. gingivalis W83 treated with polyP75 (sodium polyphosphate, Nan+2PnO3n+1; n = 75). Real-time PCR confirmed the up- and down-regulation of some selected genes. GO analysis of the DEGs identified distinct biological themes. Using 202 DEGs belonging to the biological themes, we generated the protein-protein interaction network based on a database of known and predicted protein interactions. The

Gln-70, which is located near the active-site metal, is conserved in aligned amino acid sequences of iron-containing superoxide dimutases (Fe-SODs) and cambialistic SOD from Porphyromonas gingivalis, but is complementarily substituted with Gln-142 in manganese-containing SODs (Mn-SODs). In order to clarify the contribution of this exchange of Gln to the metal-specific activity of P. gingivalis SOD, we have prepared a mutant of the enzyme with conversions of Gln-70 to Gly and Ala-142 to Gln. The ratio of the specific activities of Mn- to Fe-reconstituted P. gingivalis SOD increased from 1.4 in the wild-type to 3.5 in the mutant SODs. Furthermore, the visible absorption spectra of the Mn- and Fe-reconstituted mutant SODs more closely resembled that of Mn-specific SOD than that of the wild-type SOD. We conclude that a difference in configuration of the Gln residues of P. gingivalis SOD partially accounts for the metal-specific activity of the enzyme.. ...

Download Free Full-Text of an article Study of Porphyromonas gingivalis in periodontal diseases: A systematic review and meta-analysis

Oral mucosa provides the first line of defense against a diverse array of environmental and microbial irritants by forming the barrier of epithelial cells interconnected by multiprotein tight junctions (TJ), adherens junctions, desmosomes, and gap junction complexes. Grainyhead-like 2 (GRHL2), an epithelial-specific transcription factor, may play a role in the formation of the mucosal epithelial barrier, as it regulates the expression of the junction proteins. The current study investigated the role of GRHL2 in the Porphyromonas gingivalis (Pg)-induced impairment of epithelial barrier functions. Exposure of human oral keratinocytes (HOK-16B and OKF6 cells) to Pg or Pg-derived lipopolysaccharides (Pg LPSs) led to rapid loss of endogenous GRHL2 and the junction proteins (e.g., zonula occludens, E-cadherin, claudins, and occludin). GRHL2 directly regulated the expression levels of the junction proteins and the epithelial permeability for small molecules (e.g., dextrans and Pg bacteria). To explore ...

Summary The sequence of events involved in haemagglutination and lysis of erythrocytes by washed cells, vesicles and the culture supernate of Porphyromonas gingivalis strain W83 was monitored by 51Cr release and transmission electronmicroscopy. All preparations, except capsular material and lipopolysaccharide, caused haemagglutination and, by a slow process of attachment and specific attack on the surface structures of the red blood cells, produced minute pores and eventual leakage of cellular contents. N-acetylglucosamine, N-acetylgalactosamine and several other sugars such as glucose and sucrose had no effect on haemagglutination. Antiserum raised against a cloned haemagglutinin of P. gingivalis strain 381 inhibited the activity of strain W83 cells, vesicles and supernate. The antiserum-neutralised supernate lost 70-80% of its hydrolytic activity towards α-N-benzoyl-L-arginine-4-nitroanilide but the residual activity behaved in a manner similar to the native supernate in that it was completely

Looking for online definition of sulcus gingivalis in the Medical Dictionary? sulcus gingivalis explanation free. What is sulcus gingivalis? Meaning of sulcus gingivalis medical term. What does sulcus gingivalis mean?

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Three-dimensional (3D) printing has been applied extensively not only in human, but also veterinary medicine. However, the technique is still used in the clinical area for a surgical plan or education prior to surgery. Thus, we report a case of reconstruction after tumor removal surgery with the use of a 3D-printed scaffold. A 12-year-old female mixed dog had a left caudal maxillary mass. Based on computed tomography images, a defect was confirmed on the maxillary bone due to the oral mass, and a surgical plan was designed to remove the oral mass and graft the 3D printed scaffold ...

Affiliation (Current)：東京医科歯科大学,大学院医歯学総合研究科,准教授, Research Field：Conservative dentistry,Periodontal dentistry,Periodontal dentistry, Keywords：歯周病原性細菌,歯周疾患,Porphyromonas gingivalis,ELISA法,歯周炎,歯周組織,ICAM-1,VCAM-1,成人性歯周炎,歯周病, # of Research Projects：16, # of Research Products：43

Ultrastructure of the AgB oligomers analyzed by TEM.TEM images from rAgB8/1 (A), rAgB8/2 (B), rAgB8/3 (C), and AgB (D) oligomers. Recombinant AgB subunits were

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