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Pesquisa : B03.353.750.737.872.875.600 [Categoria DeCS]
Referências encontradas : 364 [refinar]
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[PMID]:28796424
[Au] Autor:Görl J; Possiel C; Sotriffer C; Seibel J
[Ad] Endereço:Department of Organic Chemistry, Universität Würzburg, Am Hubland, 97074, Würzburg, Germany.
[Ti] Título:Extending the Scope of GTFR Glucosylation Reactions with Tosylated Substrates for Rare Sugars Synthesis.
[So] Source:Chembiochem;18(20):2012-2015, 2017 Oct 18.
[Is] ISSN:1439-7633
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Functionalized rare sugars were synthesized with 2-, 3-, and 6-tosylated glucose derivatives as acceptor substrates by transglucosylation with sucrose and the glucansucrase GTFR from Streptococcus oralis. The 2- and 3-tosylated glucose derivatives yielded the corresponding 1,6-linked disaccharides (isomaltose analogues), whereas the 6-tosylated glucose derivatives resulted in 1,3-linked disaccharides (nigerose analogue) with high regioselectivity in up to 95 % yield. Docking studies provided insight into the binding mode of the acceptors and suggested two different orientations that were responsible for the change in regioselectivity.
[Mh] Termos MeSH primário: Glucose/síntese química
Glicosiltransferases/metabolismo
[Mh] Termos MeSH secundário: Técnicas de Química Sintética
Glucose/química
Glucose/metabolismo
Glicosilação
Glicosiltransferases/química
Simulação de Acoplamento Molecular
Conformação Proteica
Streptococcus oralis/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.4.- (Glycosyltransferases); EC 2.4.1.140 (alternansucrase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170811
[St] Status:MEDLINE
[do] DOI:10.1002/cbic.201700320


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[PMID]:28202416
[Au] Autor:Matsushima H; Kumagai Y; Vandenbon A; Kataoka H; Kadena M; Fukamachi H; Arimoto T; Morisaki H; Fujiwara N; Okahashi N; Kuwata H
[Ad] Endereço:Department of Oral Microbiology and Immunology, School of Dentistry, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan; Department of Pediatric Dentistry, School of Dentistry, Showa University, 2-1-1 Kitasenzoku, Ohta-ku, Tokyo 145-8515, Japan.
[Ti] Título:Microarray analysis of macrophage response to infection with Streptococcus oralis reveals the immunosuppressive effect of hydrogen peroxide.
[So] Source:Biochem Biophys Res Commun;485(2):461-467, 2017 Apr 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oral streptococci including mitis group streptococci are commensal residents and are also the first to colonize the oral cavity. However, various species of these oral streptococci have the potential to invade the host and occasionally lead to severe infectious disease such as cardiovascular diseases. Oral streptococci have close interactions with the host immune system including macrophages at the oral mucosal surface. One notable common trait of oral streptococcus including Streptococcus oralis (S. oralis) is the production of hydrogen peroxide (H O ). Using a comprehensive microarray approach, we sought to understand the innate immune response profiling affected by H O production from oral streptococci. We compared the gene expression patterns of macrophages infected with S. oralis wild type (WT) and streptococcal pyruvate oxidase knockout (SpxB-KO), a strain that does not produce H O . We found that H O from S. oralis suppressed proinflammatory gene expression such as TNF-α, that is induced in response to infection, and activated the cellular stress genes such as Egr-1 in response to oxidative stress. A comparative gene ontology analysis of S. oralis WT and SpxB-KO strains revealed that during infection, down regulated genes were closely related to the processes involved in the host defense reaction and up regulated genes were related with the cellular stress responses. Using qPCR analysis, we also confirmed the same pattern of expression changes such as TNF-α, IL-6 and Egr-1. Furthermore, supernatant from SpxB-KO could not suppress the expression of TNF-α in macrophages stimulated with LPS. These findings suggested that H O production from S. oralis leads to the suppression of inflammatory responses and NF-κB signaling pathways in macrophages as well as the induction of the oxidative stress response. We concluded that streptococcal H O production has the beneficial effects of modulating the innate immune response, thereby stabilizing streptococcal colonization at the mucosal surface and even in the bloodstream leading to cardiovascular disease after invasion, in addition to the commensal role to compete other bacterial species as initial colonizer at oral cavity.
[Mh] Termos MeSH primário: Perfilação da Expressão Gênica/métodos
Peróxido de Hidrogênio/metabolismo
Macrófagos/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos/métodos
Streptococcus oralis/metabolismo
[Mh] Termos MeSH secundário: Células 3T3
Animais
Proteínas de Bactérias/genética
Proteínas de Bactérias/metabolismo
Western Blotting
Linhagem Celular
Análise por Conglomerados
Proteína 1 de Resposta de Crescimento Precoce/genética
Proteína 1 de Resposta de Crescimento Precoce/metabolismo
Ontologia Genética
Interações Hospedeiro-Patógeno
Interleucina-6/genética
Interleucina-6/metabolismo
Lipopolissacarídeos/farmacologia
Macrófagos/efeitos dos fármacos
Macrófagos/microbiologia
Camundongos
Camundongos Endogâmicos BALB C
Mutação
Piruvato Oxidase/genética
Piruvato Oxidase/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Streptococcus oralis/genética
Streptococcus oralis/fisiologia
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Early Growth Response Protein 1); 0 (Egr1 protein, mouse); 0 (Interleukin-6); 0 (Lipopolysaccharides); 0 (Tumor Necrosis Factor-alpha); BBX060AN9V (Hydrogen Peroxide); EC 1.2.3.3 (Pyruvate Oxidase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170217
[St] Status:MEDLINE


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[PMID]:28115347
[Au] Autor:Mishra NN; Tran TT; Seepersaud R; Garcia-de-la-Maria C; Faull K; Yoon A; Proctor R; Miro JM; Rybak MJ; Bayer AS; Arias CA; Sullam PM
[Ad] Endereço:LA Biomedical Research Institute, Torrance, California, USA.
[Ti] Título:Perturbations of Phosphatidate Cytidylyltransferase (CdsA) Mediate Daptomycin Resistance in Streptococcus mitis/oralis by a Novel Mechanism.
[So] Source:Antimicrob Agents Chemother;61(4), 2017 Apr.
[Is] ISSN:1098-6596
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:is an important pathogen, causing life-threatening infections such as endocarditis and severe sepsis in immunocompromised patients. The ß-lactam antibiotics are the usual therapy of choice for this organism, but their effectiveness is threatened by the frequent emergence of resistance. The lipopeptide daptomycin (DAP) has been suggested for therapy against such resistant strains due to its bactericidal activity and demonstrated efficacy against other Gram-positive pathogens. Unlike other bacteria, however, has the unique ability to rapidly develop stable, high-level resistance to DAP upon exposure to the drug both and Using isogenic DAP-susceptible and DAP-resistant strain pairs, we describe a mechanism of resistance to both DAP and cationic antimicrobial peptides that involves loss-of-function mutations in (encoding a phosphatidate cytidylyltransferase). CdsA catalyzes the synthesis of cytidine diphosphate-diacylglycerol, an essential phospholipid intermediate for the production of membrane phosphatidylglycerol and cardiolipin. DAP-resistant strains demonstrated a total disappearance of phosphatidylglycerol, cardiolipin, and anionic phospholipid microdomains from membranes. In addition, these strains exhibited cross-resistance to cationic antimicrobial peptides from human neutrophils (i.e., hNP-1). Interestingly, CdsA-mediated changes in phospholipid metabolism were associated with DAP hyperaccumulation in a small subset of the bacterial population, without any binding by the remaining larger population. Our results indicate that CdsA is the major mediator of high-level DAP resistance in and suggest a novel mechanism of bacterial survival against attack by antimicrobial peptides of both innate and exogenous origins.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Daptomicina/farmacologia
Nucleotidiltransferases/metabolismo
Streptococcus oralis/efeitos dos fármacos
Streptococcus oralis/enzimologia
[Mh] Termos MeSH secundário: Cistina Difosfato/metabolismo
Farmacorresistência Bacteriana/genética
Bactérias Gram-Positivas/efeitos dos fármacos
Bactérias Gram-Positivas/enzimologia
Testes de Sensibilidade Microbiana
Neutrófilos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 63-38-7 (Cytidine Diphosphate); EC 2.7.7.- (Nucleotidyltransferases); EC 2.7.7.41 (phosphatidate cytidylyltransferase); NWQ5N31VKK (Daptomycin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170125
[St] Status:MEDLINE


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[PMID]:27993975
[Au] Autor:Singh AK; Woodiga SA; Grau MA; King SJ
[Ad] Endereço:Center for Microbial Pathogenesis, Nationwide Children's Hospital, Columbus, Ohio, USA.
[Ti] Título:Streptococcus oralis Neuraminidase Modulates Adherence to Multiple Carbohydrates on Platelets.
[So] Source:Infect Immun;85(3), 2017 Mar.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adherence to host surfaces is often mediated by bacterial binding to surface carbohydrates. Although it is widely appreciated that some bacterial species express glycosidases, previous studies have not considered whether bacteria bind to multiple carbohydrates within host glycans as they are modified by bacterial glycosidases. is a leading cause of subacute infective endocarditis. Binding to platelets is a critical step in disease; however, the mechanisms utilized by remain largely undefined. Studies revealed that , like and , binds platelets via terminal sialic acid. However, unlike those organisms, produces a neuraminidase, NanA, which cleaves terminal sialic acid. Further studies revealed that following NanA-dependent removal of terminal sialic acid, bound exposed ß-1,4-linked galactose. Adherence to both these carbohydrates required Fap1, the member of the serine-rich repeat protein (SRRP) family of adhesins. Mutation of a conserved residue required for sialic acid binding by other SRRPs significantly reduced platelet binding, supporting the hypothesis that Fap1 binds this carbohydrate. The mechanism by which Fap1 contributes to ß-1,4-linked galactose binding remains to be defined; however, binding may occur via additional domains of unknown function within the nonrepeat region, one of which shares some similarity with a carbohydrate binding module. This study is the first demonstration that an SRRP is required to bind ß-1,4-linked galactose and the first time that one of these adhesins has been shown to be required for binding of multiple glycan receptors.
[Mh] Termos MeSH primário: Aderência Bacteriana
Proteínas de Bactérias/metabolismo
Plaquetas/metabolismo
Plaquetas/microbiologia
Neuraminidase/metabolismo
Streptococcus oralis/fisiologia
[Mh] Termos MeSH secundário: Galactose/metabolismo
Seres Humanos
Ácido N-Acetilneuramínico/metabolismo
Ligação Proteica
Receptores de Superfície Celular/metabolismo
Streptococcus oralis/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Receptors, Cell Surface); EC 3.2.1.18 (Neuraminidase); GZP2782OP0 (N-Acetylneuraminic Acid); X2RN3Q8DNE (Galactose)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE


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[PMID]:26834007
[Au] Autor:Cavalcanti IM; Del Bel Cury AA; Jenkinson HF; Nobbs AH
[Ad] Endereço:Department of Prosthodontics and Periodontology, Piracicaba Dental School - University of Campinas, Piracicaba, São Paulo, Brazil.
[Ti] Título:Interactions between Streptococcus oralis, Actinomyces oris, and Candida albicans in the development of multispecies oral microbial biofilms on salivary pellicle.
[So] Source:Mol Oral Microbiol;32(1):60-73, 2017 Feb.
[Is] ISSN:2041-1014
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:The fungus Candida albicans is carried orally and causes a range of superficial infections that may become systemic. Oral bacteria Actinomyces oris and Streptococcus oralis are abundant in early dental plaque and on oral mucosa. The aims of this study were to determine the mechanisms by which S. oralis and A. oris interact with each other and with C. albicans in biofilm development. Spatial distribution of microorganisms was visualized by confocal laser scanning microscopy of biofilms labeled by differential fluorescence or by fluorescence in situ hybridization (FISH). Actinomyces oris and S. oralis formed robust dual-species biofilms, or three-species biofilms with C. albicans. The bacterial components tended to dominate the lower levels of the biofilms while C. albicans occupied the upper levels. Non-fimbriated A. oris was compromised in biofilm formation in the absence or presence of streptococci, but was incorporated into upper biofilm layers through binding to C. albicans. Biofilm growth and hyphal filament production by C. albicans was enhanced by S. oralis. It is suggested that the interkingdom biofilms are metabolically coordinated to house all three components, and this study demonstrates that adhesive interactions between them determine spatial distribution and biofilm architecture. The physical and chemical communication processes occurring in these communities potentially augment C. albicans persistence at multiple oral cavity sites.
[Mh] Termos MeSH primário: Actinomyces/fisiologia
Biofilmes/crescimento & desenvolvimento
Candida albicans/fisiologia
Película Dentária/microbiologia
Streptococcus oralis/fisiologia
[Mh] Termos MeSH secundário: Actinomyces/crescimento & desenvolvimento
Actinomyces/metabolismo
Aderência Bacteriana
Biofilmes/classificação
Candida albicans/crescimento & desenvolvimento
Candida albicans/metabolismo
Película Dentária/diagnóstico por imagem
Placa Dentária/microbiologia
Seres Humanos
Hibridização in Situ Fluorescente/métodos
Interações Microbianas
Microscopia Confocal
Boca/microbiologia
Mucosa Bucal/microbiologia
Streptococcus oralis/crescimento & desenvolvimento
Streptococcus oralis/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:D
[Da] Data de entrada para processamento:160203
[St] Status:MEDLINE
[do] DOI:10.1111/omi.12154


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[PMID]:27824896
[Au] Autor:Men X; Shibata Y; Takeshita T; Yamashita Y
[Ad] Endereço:Section of Preventive and Public Health Dentistry, Division of Oral Health, Growth and Development, Faculty of Dental Science, Kyushu University, Fukuoka, Japan.
[Ti] Título:Identification of Anion Channels Responsible for Fluoride Resistance in Oral Streptococci.
[So] Source:PLoS One;11(11):e0165900, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recently, it has been reported that eriC and crcB are involved in bacterial fluoride resistance. However, the fluoride-resistance mechanism in oral streptococci remains unclear. BLAST studies showed that two types of eriCs (eriC1 and eriC2) and two types of crcBs (crcB1 and crcB2) are present across 18 oral streptococci, which were identified in ≥ 10% of 166 orally healthy subjects with ≥ 0.01% of the mean relative abundance. They were divided into three groups based on the distribution of these four genes: group I, only eriC1; group II, eriC1 and eriC2; and group III, eriC2, crcB1, and crcB2. Group I consisted of Streptococcus mutans, in which one of the two eriC1s predominantly affected fluoride resistance. Group II consisted of eight species, and eriC1 was responsible for fluoride resistance, but eriC2 was not, in Streptococcus anginosus as a representative species. Group III consisted of nine species, and both crcB1 and crcB2 were crucial for fluoride resistance, but eriC2 was not, in Streptococcus sanguinis as a representative species. Based on these results, either EriC1 or CrcBs play a role in fluoride resistance in oral streptococci. Complementation between S. mutans EriC1 and S. sanguinis CrcB1/CrcB2 was confirmed in both S. mutans and S. sanguinis. However, neither transfer of S. sanguinis CrcB1/CrcB2 into wild-type S. mutans nor S. mutans EriC1 into wild-type S. sanguinis increased the fluoride resistance of the wild-type strain. Co-existence of different F- channels (EriC and CrcB) did not cause the additive effect on fluoride resistance in oral Streptococcus species.
[Mh] Termos MeSH primário: Fluoretos/farmacologia
Canais Iônicos/fisiologia
Streptococcus/efeitos dos fármacos
[Mh] Termos MeSH secundário: Farmacorresistência Bacteriana/genética
Genes Bacterianos/genética
Seres Humanos
Canais Iônicos/genética
Boca/microbiologia
Streptococcus/genética
Streptococcus anginosus/efeitos dos fármacos
Streptococcus anginosus/genética
Streptococcus gordonii/efeitos dos fármacos
Streptococcus gordonii/genética
Streptococcus intermedius/efeitos dos fármacos
Streptococcus intermedius/genética
Streptococcus mutans/efeitos dos fármacos
Streptococcus mutans/genética
Streptococcus oralis/efeitos dos fármacos
Streptococcus oralis/genética
Streptococcus salivarius/efeitos dos fármacos
Streptococcus salivarius/genética
Streptococcus sobrinus/efeitos dos fármacos
Streptococcus sobrinus/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ion Channels); Q80VPU408O (Fluorides)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170706
[Lr] Data última revisão:
170706
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161109
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0165900


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[PMID]:27643392
[Au] Autor:Jung JE; Cai JN; Cho SD; Song KY; Jeon JG
[Ad] Endereço:a Department of Preventive Dentistry, School of Dentistry, Institute of Oral Bioscience and BK 21 Plus Program , Chonbuk National University , Jeonju , Republic of Korea.
[Ti] Título:Influence of fluoride on the bacterial composition of a dual-species biofilm composed of Streptococcus mutans and Streptococcus oralis.
[So] Source:Biofouling;32(9):1079-87, 2016 Oct.
[Is] ISSN:1029-2454
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Despite the widespread use of fluoride for the prevention of dental caries, few studies have demonstrated the effects of fluoride on the bacterial composition of dental biofilms. This study investigated whether fluoride affects the proportion of Streptococcus mutans and S. oralis in mono- and dual-species biofilm models, via microbiological, biochemical, and confocal fluorescence microscope studies. Fluoride did not affect the bacterial count and bio-volume of S. mutans and S. oralis in mono-species biofilms, except for the 24-h-old S. mutans biofilms. However, fluoride reduced the proportion and bio-volume of S. mutans but did not decrease those of S. oralis during both S. oralis and S. mutans dual-species biofilm formation, which may be related to the decrease in extracellular polysaccharide formation by fluoride. These results suggest that fluoride may prevent the shift in the microbial proportion to cariogenic bacteria in dental biofilms, subsequently inhibiting the cariogenic bacteria dominant biofilm formation.
[Mh] Termos MeSH primário: Antibiose/efeitos dos fármacos
Biofilmes/efeitos dos fármacos
Fluoretos/farmacologia
Streptococcus mutans/efeitos dos fármacos
Streptococcus oralis/efeitos dos fármacos
[Mh] Termos MeSH secundário: Carga Bacteriana/efeitos dos fármacos
Cárie Dentária/microbiologia
Relação Dose-Resposta a Droga
Seres Humanos
Modelos Biológicos
Streptococcus mutans/crescimento & desenvolvimento
Streptococcus mutans/fisiologia
Streptococcus oralis/crescimento & desenvolvimento
Streptococcus oralis/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
Q80VPU408O (Fluorides)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160920
[St] Status:MEDLINE
[do] DOI:10.1080/08927014.2016.1230607


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[PMID]:27534397
[Au] Autor:Jensen A; Scholz CF; Kilian M
[Ad] Endereço:1​Department of Biomedicine, Aarhus University, Wilhelm Meyers Allé 4, Aarhus 8000, Denmark.
[Ti] Título:Re-evaluation of the taxonomy of the Mitis group of the genus Streptococcus based on whole genome phylogenetic analyses, and proposed reclassification of Streptococcus dentisani as Streptococcus oralis subsp. dentisani comb. nov., Streptococcus tigurinus as Streptococcus oralis subsp. tigurinus comb. nov., and Streptococcus oligofermentans as a later synonym of Streptococcus cristatus.
[So] Source:Int J Syst Evol Microbiol;66(11):4803-4820, 2016 Nov.
[Is] ISSN:1466-5034
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The Mitis group of the genus Streptococcus currently comprises 20 species with validly published names, including the pathogen S. pneumoniae. They have been the subject of much taxonomic confusion, due to phenotypic overlap and genetic heterogeneity, which has hampered a full appreciation of their clinical significance. The purpose of this study was to critically re-examine the taxonomy of the Mitis group using 195 publicly available genomes, including designated type strains for phylogenetic analyses based on core genomes, multilocus sequences and 16S rRNA gene sequences, combined with estimates of average nucleotide identity (ANI) and in silico and in vitro analyses of specific phenotypic characteristics. Our core genomic phylogenetic analyses revealed distinct clades that, to some extent, and from the clustering of type strains represent known species. However, many of the genomes have been incorrectly identified adding to the current confusion. Furthermore, our data show that 16S rRNA gene sequences and ANI are unsuitable for identifying and circumscribing new species of the Mitis group of the genus Streptococci. Based on the clustering patterns resulting from core genome phylogenetic analysis, we conclude that S. oligofermentans is a later synonym of S. cristatus. The recently described strains of the species Streptococcus dentisani includes one previously referred to as 'S. mitis biovar 2'. Together with S. oralis, S. dentisani and S. tigurinus form subclusters within a coherent phylogenetic clade. We propose that the species S. oralis consists of three subspecies: S. oralis subsp. oralis subsp. nov., S. oralis subsp. tigurinus comb. nov., and S. oralis subsp. dentisani comb. nov.
[Mh] Termos MeSH primário: Filogenia
Streptococcus oralis/classificação
Streptococcus/classificação
[Mh] Termos MeSH secundário: Técnicas de Tipagem Bacteriana
DNA Bacteriano/genética
Tipagem de Sequências Multilocus
RNA Ribossômico 16S/genética
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Bacterial); 0 (RNA, Ribosomal, 16S)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160819
[St] Status:MEDLINE
[do] DOI:10.1099/ijsem.0.001433


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[PMID]:27232358
[Au] Autor:Ferreira Ribeiro C; Cogo-Müller K; Franco GC; Silva-Concílio LR; Sampaio Campos M; de Mello Rode S; Claro Neves AC
[Ad] Endereço:Department of Prosthodontics, Dentistry School, University of Taubaté Rua: Expedicionário Ernesto Pereira, 110 Centro, Taubaté, SP 12020-330, Brazil.
[Ti] Título:Initial oral biofilm formation on titanium implants with different surface treatments: An in vivo study.
[So] Source:Arch Oral Biol;69:33-9, 2016 Sep.
[Is] ISSN:1879-1506
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The aim of this study was to examine in vivo the initial bacterial adhesion on titanium implants with different surface treatments. DESIGN: Ten subjects wore oral splints containing machined pure titanium disks (Ti-M), acid-etched titanium (Ti-AE) and anodized and laser irradiated disks (Ti-AL) for 24h. After this period, disks were removed from the splints and adherent bacteria were quantified by an enzymatic assay to assess total viable bacteria and by Real Time PCR to evaluate total bacteria and Streptococcus oralis levels. Additionally, the initial adherent microorganisms were visualized by scanning electron microscopy (SEM). Titanium surface morphology was verified using SEM, and roughness was evaluated by profilometer analysis. RESULTS: Regarding titanium surface roughness, Ti-AL (1.423±0.397) showed significantly higher Ra values than did Ti-M (0.771±0.182) and Ti-AE (0.735±0.196) (p<0.05, ANOVA - Tahame). Ti-AE and Ti-AL presented roughened micro-structure surfaces characterized by open pores, whereas Ti-M showed long grooves alternating with planed areas. Comparing the Ti-M, Ti-AE and Ti-AL groups for viable bacteria (MTT assay), total bacteria and S. oralis quantification (qPCR), no significant differences were observed among these three groups (p>0.05, ANOVA - Tahame). SEM images showed similar bacterial adhesion on the three titanium surfaces, predominantly characterized by cocci and several bacilli, indicating an initial colonization of the oral biofilm. CONCLUSION: In conclusion, roughness and microtopography did not stimulate initial biofilm formation on titanium surfaces with different surface treatments.
[Mh] Termos MeSH primário: Biofilmes/crescimento & desenvolvimento
Implantes Dentários/microbiologia
Titânio
[Mh] Termos MeSH secundário: Ataque Ácido Dentário/métodos
Aderência Bacteriana
Técnicas Eletroquímicas
Seres Humanos
Lasers
Teste de Materiais
Microscopia Eletrônica de Varredura
Reação em Cadeia da Polimerase em Tempo Real
Streptococcus oralis/fisiologia
Propriedades de Superfície
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dental Implants); D1JT611TNE (Titanium)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170316
[Lr] Data última revisão:
170316
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:160528
[St] Status:MEDLINE


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[PMID]:27190184
[Au] Autor:Xu H; Sobue T; Bertolini M; Thompson A; Dongari-Bagtzoglou A
[Ad] Endereço:Department of Oral Health and Diagnostic Sciences, School of Dental Medicine, University of Connecticut, Farmington.
[Ti] Título:Streptococcus oralis and Candida albicans Synergistically Activate µ-Calpain to Degrade E-cadherin From Oral Epithelial Junctions.
[So] Source:J Infect Dis;214(6):925-34, 2016 Sep 15.
[Is] ISSN:1537-6613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Streptococcus oralis forms robust mucosal biofilms with Candida albicans that have increased pathogenic potential. In this study, using oral epithelial cultures, organotypic oral mucosal constructs, and a mouse model of oral infection, we demonstrated that S. oralis augmented C. albicans invasion through epithelial junctions. C. albicans and S. oralis decreased epithelial E-cadherin levels by synergistically increasing µ-calpain, a proteolytic enzyme that targets E-cadherin. In the mouse coinfection model this was accompanied by increased fungal kidney dissemination. Coinfection with a secreted aspartyl protease (sap) mutant sap2456 and S. oralis increased µ-calpain and triggered mucosal invasion and systemic dissemination, suggesting that fungal protease activity is not required for invasion during coinfection. We conclude that C. albicans and S. oralis synergize to activate host enzymes that cleave epithelial junction proteins and increase fungal invasion.
[Mh] Termos MeSH primário: Caderinas/metabolismo
Calpaína/metabolismo
Candida albicans/fisiologia
Interações Microbianas
Streptococcus oralis/fisiologia
[Mh] Termos MeSH secundário: Animais
Candidíase Bucal/microbiologia
Candidíase Bucal/patologia
Células Cultivadas
Modelos Animais de Doenças
Células Epiteliais/microbiologia
Células Epiteliais/fisiologia
Feminino
Camundongos Endogâmicos C57BL
Proteólise
Infecções Estreptocócicas/microbiologia
Infecções Estreptocócicas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (E-cadherin protein, mouse); EC 3.4.22.- (Calpain); EC 3.4.22.- (mu-calpain)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160519
[St] Status:MEDLINE
[do] DOI:10.1093/infdis/jiw201



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