scholarly journals The Surface Layer of Tannerella forsythia Contributes to Serum Resistance and Oral Bacterial Coaggregation

2013 ◽  
Vol 81 (4) ◽  
pp. 1198-1206 ◽  
Author(s):  
Naohiro Shimotahira ◽  
Yuichi Oogai ◽  
Miki Kawada-Matsuo ◽  
Sakuo Yamada ◽  
Kenji Fukutsuji ◽  
...  
Keyword(s):  
Surface Layer ◽  
Calf Serum ◽  
Fusobacterium Nucleatum ◽  
Oral Bacteria ◽  
Multiple Roles ◽  
Serum Resistance ◽  
Survival Ratio ◽  
Wild Type ◽  
Tannerella Forsythia ◽  
Content Type

ABSTRACTTannerella forsythiais an anaerobic, Gram-negative bacterium involved in the so-called “red complex,” which is associated with severe and chronic periodontitis. The surface layer (S-layer) ofT. forsythiais composed of cell surface glycoproteins, such as TfsA and TfsB, and is known to play a role in adhesion/invasion and suppression of proinflammatory cytokine expression. Here we investigated the association of this S-layer with serum resistance and coaggregation with other oral bacteria. The growth of the S-layer-deficient mutant in a bacterial medium containing more than 20% non-heat-inactivated calf serum (CS) or more than 40% non-heat-inactivated human serum was significantly suppressed relative to that of the wild type (WT). Next, we used confocal microscopy to perform quantitative analysis on the effect of serum. The survival ratio of the mutant exposed to 100% non-heat-inactivated CS (76% survival) was significantly lower than that of the WT (97% survival). Furthermore, significant C3b deposition was observed in the mutant but not in the WT. In a coaggregation assay, the mutant showed reduced coaggregation withStreptococcus sanguinis,Streptococcus salivarius, andPorphyromonas gingivalisbut strong coaggregation withFusobacterium nucleatum. These results indicated that the S-layer ofT. forsythiaplays multiple roles in virulence and may be associated with periodontitis.

scholarly journals Structure and Immunogenicity of the Rough-Type Lipopolysaccharide from the Periodontal Pathogen Tannerella forsythia

2013 ◽  
Vol 20 (6) ◽  
pp. 945-953 ◽  
Author(s):  
Gerald Posch ◽  
Oleh Andrukhov ◽  
Evgeny Vinogradov ◽  
Buko Lindner ◽  
Paul Messner ◽  
...  
Keyword(s):  
Surface Layer ◽  
Interleukin 1 ◽  
Calf Serum ◽  
Periodontal Pathogen ◽  
Glycan Structure ◽  
Resonance Spectroscopy ◽  
Dependent Manner ◽  
Tannerella Forsythia ◽  
Necrosis Factor Alpha ◽  
Content Type

ABSTRACTTannerella forsythiais a Gram-negative anaerobic organism that inhabits subgingival plaque biofilms and is covered with a so far unique surface layer composed of two glycoproteins. It belongs to the so-called “red complex” of bacteria comprising species that are associated with periodontal disease. While the surface layer glycoprotein glycan structure had been elucidated recently and found to be a virulence factor, no structural data on the lipopolysaccharide (LPS) of this organism were available. In this study, theT. forsythiaLPS structure was partially elucidated by a combined mass spectrometry (MS) and nuclear magnetic resonance spectroscopy (NMR) approach and initial experiments to characterize its immunostimulatory potential were performed. TheT. forsythiaLPS is a complex, rough-type LPS with a core region composed of one 3-deoxy-d-manno-oct-2-ulosonic acid (Kdo) residue, three mannose residues, and two glucosamine residues. MS analyses of O-deacylated LPS proved that, in addition, one phosphoethanolamine residue and most likely one galactose-phosphate residue were present, however, their positions could not be identified. Stimulation of human macrophages withT. forsythiaLPS resulted in the production of the proinflammatory cytokines interleukin-1 (IL-1), IL-6, and tumor necrosis factor alpha in a dose-dependent manner. The response toT. forsythiaLPS was observed only upon stimulation in the presence of fetal calf serum (FCS), whereas no cytokine production was observed in the absence of FCS. This finding suggests that the presence of certain additional cofactors is crucial for the immune response induced byT. forsythiaLPS.

Fretibacterium fastidiosum gen. nov., sp. nov., isolated from the human oral cavity

2013 ◽  
Vol 63 (Pt_2) ◽  
pp. 458-463 ◽  
Author(s):  
Sonia R. Vartoukian ◽  
Julia Downes ◽  
Richard M. Palmer ◽  
William G. Wade
Keyword(s):  
New Genus ◽  
Novel Species ◽  
Fusobacterium Nucleatum ◽  
Oral Bacteria ◽  
Rrna Gene ◽  
Good Growth ◽  
Content Type ◽  
Cellular Fatty Acids ◽  
Link Type ◽  
Peptone Yeast Extract Glucose

SGP1T, a strain belonging to a lineage of the phylum Synergistetes with no previously cultivated representatives was subjected to a comprehensive range of phenotypic and genotypic tests. For good growth the strain was dependent on co-culture with, or extracts from, selected other oral bacteria. Cells of strain SGP1T were asaccharolytic and major amounts of acetic acid and moderate amounts of propionic acid were produced as end products of metabolism in peptone-yeast extract-glucose broth supplemented with a filtered cell sonicate of Fusobacterium nucleatum subsp. nucleatum ATCC 25586T (25 %, v/v). Hydrogen sulphide was produced and gelatin was weakly hydrolysed. The major cellular fatty acids were C14 : 0, C18 : 0 and C16 : 0. The DNA G+C content of strain SGP1T was 63 mol%. Phylogenetic analysis of the full-length 16S rRNA gene showed that strain SGP1T represented a novel group within the phylum Synergistetes . A novel species in a new genus, Fretibacterium fastidiosum gen. nov., sp. nov., is proposed. The type strain of Fretibacterium fastidiosum is SGP1T ( = DSM 25557T = JCM 16858T).

scholarly journals β-Glucanase Activity of the Oral Bacterium Tannerella forsythia Contributes to the Growth of a Partner Species, Fusobacterium nucleatum, in Cobiofilms

2017 ◽  
Vol 84 (1) ◽  
Author(s):  
Kiyonobu Honma ◽  
Angela Ruscitto ◽  
Ashu Sharma
Keyword(s):  
Periodontal Disease ◽  
Sigma Factor ◽  
Dental Plaque ◽  
Fusobacterium Nucleatum ◽  
Disease Pathogenesis ◽  
Glucanase Activity ◽  
Tannerella Forsythia ◽  
Content Type ◽  
Plaque Development ◽  
Oral Bacterium

ABSTRACTTannerella forsythiaandFusobacterium nucleatumare dental plaque bacteria implicated in the development of periodontitis. These two species have been shown to form synergistic biofilms and have been found to be closely associated in dental plaque biofilms. A number of genetic loci for TonB-dependent membrane receptors (TDR) for glycan acquisition, with many existing in association with genes coding for enzymes involved in the breakdown of complex glycans, have been identified inT. forsythia. In this study, we focused on a locus, BFO_0186-BFO_0188, that codes for a predicted TDR-SusD transporter along with a putative β-glucan hydrolyzing enzyme (BFO_0186). This operon is located immediately downstream of a 2-gene operon that codes for a putative stress-responsive extracytoplasmic function (ECF) sigma factor and an anti-sigma factor. Here, we show that BFO_0186 expresses a β-glucanase that cleaves glucans with β-1,6 and β-1,3 linkages. Furthermore, the BFO_0186-BFO_0188 locus is upregulated, with an induction of β-glucanase activity, in cobiofilms ofT. forsythiaandF. nucleatum. The β-glucanase activity in mixed biofilms in turn leads to an enhanced hydrolysis of β-glucans and release of glucose monomers and oligomers as nutrients forF. nucleatum. In summary, our study highlights the role ofT. forsythiaβ-glucanase expressed by the asaccharolytic oral bacteriumT. forsythiain the development ofT. forsythia-F. nucleatummixed species biofilms, and suggest that dietary β-glucans might contribute in plaque development and periodontal disease pathogenesis.IMPORTANCEThe development of dental plaque biofilm is a complex process in which metabolic, chemical and physical interactions between bacteria take a central role. Previous studies have shown that the dental pathogensT. forsythiaandF. nucleatumform synergistic biofilms and are closely associated in human dental plaque. In this study, we show that β-glucanase from the periodontal pathogenT. forsythiaplays a role in the formation ofT. forsythia-F. nucleatumcobiofilms by hydrolyzing β-glucans to glucose as a nutrient. We also unveiled that the expression ofT. forsythiaβ-glucanase is induced in response toF. nucleatumsensing. This study highlights the involvement of β-glucanase activity in the development ofT. forsythia-F. nucleatumbiofilms and suggests that intake of dietary β-glucans might be a contributing risk factor in plaque development and periodontal disease pathogenesis.

scholarly journals Metabolic and Community Synergy of Oral Bacteria in Colorectal Cancer

mSphere ◽  
2016 ◽  
Vol 1 (3) ◽  
Author(s):  
Kaitlin J. Flynn ◽  
Nielson T. Baxter ◽  
Patrick D. Schloss
Keyword(s):  
Colorectal Cancer ◽  
Fusobacterium Nucleatum ◽  
Oral Bacteria ◽  
Oral Microbiota ◽  
Community Members ◽  
Content Type ◽  
Bacterial Physiology ◽  
Oral Biofilms ◽  
Two Factors

ABSTRACT The oral periodontopathic bacterium Fusobacterium nucleatum has been repeatedly associated with colorectal tumors. Molecular analysis has identified specific virulence factors that promote tumorigenesis in the colon. However, other oral community members, such as members of the Porphyromonas spp., are also found with F. nucleatum on colonic tumors, and thus, narrow studies of individual pathogens do not take community-wide virulence properties into account. A broader view of oral bacterial physiology and pathogenesis identifies two factors that could promote colonization and persistence of oral bacterial communities in the colon. The polymicrobial nature of oral biofilms and the asaccharolytic metabolism of many of these species make them well suited to life in the microenvironment of colonic lesions. Consideration of these two factors offers a novel perspective on the role of oral microbiota in the initiation, development, and treatment of colorectal cancer.

scholarly journals Draft Whole-Genome Sequences of Periodontal Pathobionts Porphyromonas gingivalis, Prevotella intermedia, and Tannerella forsythia Contain Phase-Variable Restriction-Modification Systems

2017 ◽  
Vol 5 (46) ◽  
Author(s):  
Richard D. Haigh ◽  
Liam A. Crawford ◽  
Joseph D. Ralph ◽  
Joseph J. Wanford ◽  
Sonia R. Vartoukian ◽  
...  
Keyword(s):  
Periodontal Disease ◽  
Porphyromonas Gingivalis ◽  
Disease Process ◽  
Oral Bacteria ◽  
Host Responses ◽  
Prevotella Intermedia ◽  
Phase Variable ◽  
Genome Sequences ◽  
Tannerella Forsythia ◽  
Content Type

ABSTRACT Periodontal disease comprises mild to severe inflammatory host responses to oral bacteria that can cause destruction of the tooth-supporting tissue. We report genome sequences for 18 clinical isolates of Porphyromonas gingivalis, Prevotella intermedia, and Tannerella forsythia, Gram-negative obligate anaerobes that play a role in the periodontal disease process.

scholarly journals Fusobacterium nucleatum and Tannerella forsythia Induce Synergistic Alveolar Bone Loss in a Mouse Periodontitis Model

2012 ◽  
Vol 80 (7) ◽  
pp. 2436-2443 ◽  
Author(s):  
Rajendra P. Settem ◽  
Ahmed Taher El-Hassan ◽  
Kiyonobu Honma ◽  
Graham P. Stafford ◽  
Ashu Sharma
Keyword(s):  
Bone Loss ◽  
Mixed Infection ◽  
Alveolar Bone ◽  
Fusobacterium Nucleatum ◽  
Single Species ◽  
Opportunistic Pathogen ◽  
Alveolar Bone Loss ◽  
Tannerella Forsythia ◽  
Content Type ◽  
Jaw Bones

ABSTRACTTannerella forsythiais strongly associated with chronic periodontitis, an inflammatory disease of the tooth-supporting tissues, leading to tooth loss.Fusobacterium nucleatum, an opportunistic pathogen, is thought to promote dental plaque formation by serving as a bridge bacterium between early- and late-colonizing species of the oral cavity. Previous studies have shown thatF. nucleatumspecies synergize withT. forsythiaduring biofilm formation and pathogenesis. In the present study, we showed that coinfection ofF. nucleatumandT. forsythiais more potent than infection with either species alone in inducing NF-κB activity and proinflammatory cytokine secretion in monocytic cells and primary murine macrophages. Moreover, in a murine model of periodontitis, mixed infection with the two species induces synergistic alveolar bone loss, characterized by bone loss which is greater than the additive alveolar bone losses induced by each species alone. Further, in comparison to the single-species infection, mixed infection caused significantly increased inflammatory cell infiltration in the gingivae and osteoclastic activity in the jaw bones. These data show thatF. nucleatumsubspecies andT. forsythiasynergistically stimulate the host immune response and induce alveolar bone loss in a murine experimental periodontitis model.

scholarly journals Pathogenic Bacterial Species Associated with Endodontic Infection Evade Innate Immune Control by Disabling Neutrophils

2014 ◽  
Vol 82 (10) ◽  
pp. 4068-4079 ◽  
Author(s):  
Aritsune Matsui ◽  
Jun-O Jin ◽  
Christopher D. Johnston ◽  
Hajime Yamazaki ◽  
Yael Houri-Haddad ◽  
...  
Keyword(s):  
Bacterial Species ◽  
Fusobacterium Nucleatum ◽  
Oral Bacteria ◽  
Innate Immune ◽  
Tooth Pulp ◽  
Content Type ◽  
Endodontic Infection ◽  
Parvimonas Micra ◽  
Endodontic Infections

ABSTRACTEndodontic infections, in which oral bacteria access the tooth pulp chamber, are common and do not resolve once established. To investigate the effects of these infections on the innate immune response, we established a mouse subcutaneous chamber model, where a mixture of four oral pathogens commonly associated with these infections (endodontic pathogens [EP]), i.e.,Fusobacterium nucleatum,Streptococcus intermedius,Parvimonas micra, andPrevotella intermedia, was inoculated into subcutaneously implanted titanium chambers. Cells that infiltrated the chamber after these infections were primarily neutrophils; however, these neutrophils were unable to control the infection. Infection with a nonpathogenic oral bacterial species,Streptococcus mitis, resulted in well-controlled infection, with bacterial numbers reduced by 4 to 5 log units after 7 days. Propidium iodide (PI) staining of the chamber neutrophils identified three distinct populations: neutrophils from EP-infected chambers were intermediate in PI staining, while cells in chambers from mice infected withS. mitiswere PI positive (apoptotic) or negative (live). Strikingly, neutrophils from EP-infected chambers were severely impaired in their ability to phagocytose and to generate reactive oxygen speciesin vitroafter removal from the chamber compared to cells fromS. mitis-infected chambers. The mechanism of neutrophil impairment was necrotic cell death as determined by morphological analyses.P. intermediaalone could induce a similar neutrophil phenotype. We conclude that the endodontic pathogens, particularlyP. intermedia, can efficiently disable and kill infiltrating neutrophils, allowing these infections to become established. These results can help explain the persistence of endodontic infections and demonstrate a new virulence mechanism associated withP. intermedia.

scholarly journals Fap2 of Fusobacterium nucleatum Is a Galactose-Inhibitable Adhesin Involved in Coaggregation, Cell Adhesion, and Preterm Birth

2015 ◽  
Vol 83 (3) ◽  
pp. 1104-1113 ◽  
Author(s):  
S. Coppenhagen-Glazer ◽  
A. Sol ◽  
J. Abed ◽  
R. Naor ◽  
X. Zhang ◽  
...  
Keyword(s):  
Fusobacterium Nucleatum ◽  
Host Cells ◽  
Wild Type ◽  
Cell Binding ◽  
Content Type ◽  
Log Reduction ◽  
Dental Biofilm ◽  
Gene Coding ◽  
Oral Environment ◽  
Intrauterine Infections

Fusobacterium nucleatumis a common oral anaerobe involved in periodontitis that is known to translocate and cause intrauterine infections. In the oral environment,F. nucleatumadheres to a large diversity of species, facilitating their colonization and creating biological bridges that stabilize the multispecies dental biofilm. Many of these interactions (called coadherences or coaggregations) are galactose sensitive. Galactose-sensitive interactions are also involved in the binding ofF. nucleatumto host cells. Hemagglutination of someF. nucleatumstrains is also galactose sensitive, suggesting that a single galactose-sensitive adhesin might mediate the interaction of fusobacteria with many partners and targets. In order to identify the fusobacterial galactose-sensitive adhesin, a system for transposon mutagenesis in fusobacteria was created. The mutant library was screened for hemagglutination deficiency, and three clones were isolated. All three clones were found to harbor the transposon in the gene coding for the Fap2 outer membrane autotransporter. The threefap2mutants failed to show galactose-inhibitable coaggregation withPorphyromonas gingivalisand were defective in cell binding. Afap2mutant also showed a 2-log reduction in murine placental colonization compared to that of the wild type. Our results suggest that Fap2 is a galactose-sensitive hemagglutinin and adhesin that is likely to play a role in the virulence of fusobacteria.

scholarly journals Mutations in fbiD (Rv2983) as a Novel Determinant of Resistance to Pretomanid and Delamanid in Mycobacterium tuberculosis

2020 ◽  
Vol 65 (1) ◽  
pp. e01948-20
Author(s):  
Dalin Rifat ◽  
Si-Yang Li ◽  
Thomas Ioerger ◽  
Keshav Shah ◽  
Jean-Philippe Lanoix ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Clinical Evidence ◽  
Clinical Samples ◽  
Loss Of Function ◽  
Wild Type ◽  
Content Type ◽  
Solid Media ◽  
High Level ◽  
Level Resistance

ABSTRACTThe nitroimidazole prodrugs delamanid and pretomanid comprise one of only two new antimicrobial classes approved to treat tuberculosis (TB) in 50 years. Prior in vitro studies suggest a relatively low barrier to nitroimidazole resistance in Mycobacterium tuberculosis, but clinical evidence is limited to date. We selected pretomanid-resistant M. tuberculosis mutants in two mouse models of TB using a range of pretomanid doses. The frequency of spontaneous resistance was approximately 10−5 CFU. Whole-genome sequencing of 161 resistant isolates from 47 mice revealed 99 unique mutations, of which 91% occurred in 1 of 5 genes previously associated with nitroimidazole activation and resistance, namely, fbiC (56%), fbiA (15%), ddn (12%), fgd (4%), and fbiB (4%). Nearly all mutations were unique to a single mouse and not previously identified. The remaining 9% of resistant mutants harbored mutations in Rv2983 (fbiD), a gene not previously associated with nitroimidazole resistance but recently shown to be a guanylyltransferase necessary for cofactor F420 synthesis. Most mutants exhibited high-level resistance to pretomanid and delamanid, although Rv2983 and fbiB mutants exhibited high-level pretomanid resistance but relatively small changes in delamanid susceptibility. Complementing an Rv2983 mutant with wild-type Rv2983 restored susceptibility to pretomanid and delamanid. By quantifying intracellular F420 and its precursor Fo in overexpressing and loss-of-function mutants, we provide further evidence that Rv2983 is necessary for F420 biosynthesis. Finally, Rv2983 mutants and other F420H2-deficient mutants displayed hypersusceptibility to some antibiotics and to concentrations of malachite green found in solid media used to isolate and propagate mycobacteria from clinical samples.

Sign in / Sign up

Export Citation Format

Share Document