Search results for "virulence factor"

showing 10 items of 85 documents

Legionella pneumophila pangenome reveals strain-specific virulence factors

2010

Abstract Background Legionella pneumophila subsp. pneumophila is a gram-negative γ-Proteobacterium and the causative agent of Legionnaires' disease, a form of epidemic pneumonia. It has a water-related life cycle. In industrialized cities L. pneumophila is commonly encountered in refrigeration towers and water pipes. Infection is always via infected aerosols to humans. Although many efforts have been made to eradicate Legionella from buildings, it still contaminates the water systems. The town of Alcoy (Valencian Region, Spain) has had recurrent outbreaks since 1999. The strain "Alcoy 2300/99" is a particularly persistent and recurrent strain that was isolated during one of the most signifi…

Genomic Islandslcsh:QH426-470biologyVirulence FactorsLegionellalcsh:BiotechnologyStrain (biology)OutbreakVirulenceGenomicsbiology.organism_classificationLegionella pneumophilaGenomeLegionella pneumophilaMicrobiologyEvolution Molecularlcsh:Geneticslcsh:TP248.13-248.65Horizontal gene transferGeneticsCRISPRGenome BacterialResearch ArticleBiotechnologyBMC Genomics
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Flavobacterium columnare colony types: connection to adhesion and virulence?

2008

Four different colony morphologies were produced by Flavobacterium columnare strains on Shieh agar plate cultures: rhizoid and flat (type 1), non-rhizoid and hard (type 2), round and soft (type 3), and irregularly shaped and soft (type 4). Colonies produced on AO agar differed from these to some extent. The colony types formed on Shieh agar were studied according to molecular characteristics [Amplified Fragment Length Polymorphism (AFLP), Automated Ribosomal Intergenic Spacer Analysis (ARISA), and whole cell protein SDS-PAGE profiles], virulence on rainbow trout fingerlings, and adhesion on polystyrene and fish gills. There were no molecular differences between colony types within one strai…

Gillsfood.ingredientRibosomal Intergenic Spacer analysisVirulenceBiologyMicrobiologyFlavobacteriumVirulence factorBacterial AdhesionMicrobiologyAgar plateFish DiseasesfoodBacterial ProteinsFlavobacteriaceae InfectionsDNA Ribosomal SpacerAgarAnimalsPhase variationVirulencebiology.organism_classificationCulture MediaAgarInfectious DiseasesOncorhynchus mykissFlavobacterium columnarePolystyrenesElectrophoresis Polyacrylamide GelFlavobacteriumPolymorphism Restriction Fragment LengthMicrobial pathogenesis
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Phage-driven loss of virulence in a fish pathogenic bacterium

2012

Parasites provide a selective pressure during the evolution of their hosts, and mediate a range of effects on ecological communities. Due to their short generation time, host-parasite interactions may also drive the virulence of opportunistic bacteria. This is especially relevant in systems where high densities of hosts and parasites on different trophic levels (e.g. vertebrate hosts, their bacterial pathogens, and virus parasitizing bacteria) co-exist. In farmed salmonid fingerlings, Flavobacterium columnare is an emerging pathogen, and phage that infect F. columnare have been isolated. However, the impact of these phage on their host bacterium is not well understood. To study this, four s…

Gliding motilityPathogenesisAquacultureFish DiseasesFlavobacteriaceae InfectionsSalmonphageBacteriophagesPathogenZebrafishGliding motility0303 health sciencesEvolutionary TheoryMultidisciplinarybiologyEcologyVirulenceQRFishesvirulenssiAnimal ModelsBiological EvolutionBacterial PathogensHost-Pathogen InteractionLytic cycleMedicineResearch ArticleScienceVirulenceMicrobiologyFlavobacteriumMicrobiologyMicrobial EcologyHost-Parasite Interactions03 medical and health sciencesModel OrganismsVirologyAnimals14. Life underwaterBiology030304 developmental biologyEvolutionary Biology030306 microbiologyHost (biology)ta1182biology.organism_classificationEvolutionary Ecologyphage resistanceFlavobacterium columnareVirulence Factors and Mechanismsta1181BacteriaFlavobacteriumopportunismi
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Two Host Clades, Two Bacterial Arsenals: Evolution through Gene Losses in Facultative Endosymbionts.

2015

International audience; Bacterial endosymbiosis is an important evolutionary process in insects, which can harbor both obligate and facultative symbionts. The evolution of these symbionts is driven by evolutionary convergence, and they exhibit among the tiniest genomes in prokaryotes. The large host spectrum of facultative symbionts and the high diversity of strategies they use to infect new hosts probably impact the evolution of their genome and explain why they undergo less severe genomic erosion than obligate symbionts. Candidatus Hamiltonella defensa is suitable for the investigation of the genomic evolution of facultative symbionts because the bacteria are engaged in specific relations…

Hamiltonella defensaVirulence Factors[SDV]Life Sciences [q-bio]fungifood and beveragesGenomicscomparative genomicsbiochemical phenomena metabolism and nutritionBemisia tabaciEvolution MolecularHemipteraaphidsEnterobacteriaceaeCell WallAnimals[INFO.INFO-BI]Computer Science [cs]/Bioinformatics [q-bio.QM]SymbiosisGene DeletionGenome BacterialPhylogenyResearch Article
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Suppression of CD8+ T cell recognition in the immediate-early phase of human cytomegalovirus infection.

2012

Human cytomegalovirus (HCMV) interferes with MHC class I-restricted antigen presentation and thereby reduces recognition by CD8+ T-cells. This interference is mediated primarily by endoplasmic reticulum-resident glycoproteins that are encoded in the US2–11 region of the viral genome. Such a suppression of recognition would be of particular importance immediately after infection, because several immunodominant viral antigens are already present in the cell in this phase. However, which of the evasion proteins gpUS2–11 interfere(s) with antigen presentation to CD8+ T-cells at this time of infection is not known. Here we address this question, using recombinant viruses (RV) that express only o…

Human cytomegalovirusVirulence FactorsvirusesAntigen presentationCytomegalovirusCD8-Positive T-LymphocytesCell LineImmune toleranceViral ProteinsViral Envelope ProteinsAntigenVirologyMHC class IImmune TolerancemedicineHumansCytotoxic T cellImmune EvasionbiologyHistocompatibility Antigens Class IRNA-Binding Proteinsvirus diseasesmedicine.diseaseVirologyCell cultureCytomegalovirus InfectionsImmunologybiology.proteinCD8
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2,6-Disubstituted imidazo[2,1-b][1,3,4]thiadiazole derivatives as potent staphylococcal biofilm inhibitors.

2019

Abstract A class of 36 new 2-(6-phenylimidazo[2,-1-b][1,3,4]thiadiazol-2-yl)-1H-indoles was efficiently synthesized and evaluated for their anti-biofilm properties against the Gram-positive bacterial reference strains Staphylococcus aureus ATCC 25923, S. aureus ATCC 6538 and Staphylococcus epidermidis ATCC 12228, and the Gram-negative strains Pseudomonas aeruginosa ATCC 15442 and Escherichia coli ATCC 25922. Many of these new compounds, were able to inhibit biofilm formation of the tested staphylococcal strains showing BIC50 lower than 10 μg/ml. In particular, derivatives 9c and 9h showed remarkable anti-biofilm activity against S. aureus ATCC 25923 with BIC50 values of 0.5 and 0.8 μg/ml, r…

Indoles3Anti-virulence agentStaphylococcus1-b][1Bacterial growthAnti-Biofilm agentsmedicine.disease_causeSettore BIO/19 - Microbiologia GeneraleGram-Positive Bacteriaimidazo[201 natural sciencesVirulence factorMicrobiology03 medical and health sciencesStaphylococcus epidermidisDrug DiscoveryGram-Negative BacteriaThiadiazolesmedicineStaphylococcal biofilm inhibitorsEscherichia coli030304 developmental biologyPharmacology0303 health sciences4]thiadiazole derivativesbiologyStaphylococcal biofilm inhibitorVirulenceAnti-Biofilm agents; Anti-virulence agents; imidazo[21-b][134]thiadiazole derivatives; Staphylococcal biofilm inhibitors; Anti-Bacterial Agents; Biofilms; Gram-Negative Bacteria; Gram-Positive Bacteria; Indoles; Staphylococcus; Thiadiazoles; Virulence010405 organic chemistryPseudomonas aeruginosaChemistryimidazo[21-b][134]thiadiazole derivativesOrganic ChemistryBiofilmGeneral Medicinebiology.organism_classificationSettore CHIM/08 - Chimica FarmaceuticaAnti-Biofilm agent0104 chemical sciencesAnti-Bacterial AgentsAnti-virulence agentsStaphylococcus aureusBiofilms1 3 4 thiadiazole derivativesEuropean journal of medicinal chemistry
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Global Functional Analyses of Cellular Responses to Pore-Forming Toxins

2011

Here we present the first global functional analysis of cellular responses to pore-forming toxins (PFTs). PFTs are uniquely important bacterial virulence factors, comprising the single largest class of bacterial protein toxins and being important for the pathogenesis in humans of many Gram positive and Gram negative bacteria. Their mode of action is deceptively simple, poking holes in the plasma membrane of cells. The scattered studies to date of PFT-host cell interactions indicate a handful of genes are involved in cellular defenses to PFTs. How many genes are involved in cellular defenses against PFTs and how cellular defenses are coordinated are unknown. To address these questions, we pe…

MAPK/ERK pathwayTranscription GeneticImmunology/Innate ImmunityMessengerInteractomeInfectious Diseases/Bacterial InfectionsRNA interference2.1 Biological and endogenous factorsAetiologyBiology (General)Genes HelminthCaenorhabditis elegansOligonucleotide Array Sequence AnalysisGenetics0303 health sciencesGenomebiologyReverse Transcriptase Polymerase Chain ReactionGenetics and Genomics/Functional Genomics030302 biochemistry & molecular biologyrespiratory systemCell biologyInfectious DiseasesMedical MicrobiologyRNA InterferenceSignal transductionDNA microarrayTranscriptionBiotechnologyResearch ArticleSignal TransductionPore Forming Cytotoxic ProteinsQH301-705.5Virulence FactorsMAP Kinase Signaling System1.1 Normal biological development and functioningBacterial ToxinsImmunologyMicrobiologyDNA-binding proteinCell Line03 medical and health sciencesBacterial ProteinsGeneticUnderpinning researchVirologyEscherichia coliHelminthGeneticsAnimalsHumansRNA MessengerCaenorhabditis elegansCaenorhabditis elegans ProteinsMolecular BiologyGene030304 developmental biologyGenome HelminthCell MembraneGenetics and GenomicsRC581-607biology.organism_classificationrespiratory tract diseasesTranscription Factor AP-1Emerging Infectious DiseasesGenesRNAParasitologyGeneric health relevanceRNA HelminthImmunologic diseases. AllergyPLoS Pathogens
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Virulent synergistic effect between Enterococcus faecalis and Escherichia coli assayed by using the Caenorhabditis elegans model.

2008

5 pages; International audience; BACKGROUND: The role of enterococci in the pathogenesis of polymicrobial infections is still debated. The purpose of this study was to evaluate the effect of virulent enterococci in the presence or absence of Escherichia coli strains in the in vivo Caenorhabditis elegans model. PRINCIPAL FINDINGS: This study demonstrated that there was a synergistic effect on virulence when an association of enterococci and E. coli (LT50 = 1.6 days+/-0.1 according to the tested strains and death of nematodes in 4 days+/-0.5) was tested in comparison with enterococci alone (LT50 = 4.6 days+/-0.1 and death in 10.4 days+/-0.6) or E. coli alone (LT50 = 2.1+/-0.9 and deaths 6.6+/…

MESH : Virulence FactorsInfectious Diseases/Gastrointestinal InfectionsMESH : Escherichia colilcsh:MedicineMESH : Genotypemedicine.disease_causeMESH: Regression AnalysisPathogenesisMESH: GenotypeInfectious Diseases/Bacterial InfectionsMESH : Regression AnalysisGenotype[ SDV.EE.IEO ] Life Sciences [q-bio]/Ecology environment/SymbiosisEnterococcus faecalis[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: AnimalsMESH : Anti-Bacterial AgentsMESH : Enterococcus faecalislcsh:ScienceCaenorhabditis elegans0303 health sciencesMultidisciplinarybiologyMESH: Escherichia coliBacterial Infections3. Good healthAnti-Bacterial AgentsMicrobiology/Immunity to InfectionsMESH : Bacterial InfectionsGastroenterology and Hepatology/Gastrointestinal Infections[SDV.IMM]Life Sciences [q-bio]/ImmunologyRegression AnalysisMicrobiology/Cellular Microbiology and PathogenesisResearch ArticleMESH: Enterococcus faecalis[SDV.IMM] Life Sciences [q-bio]/ImmunologyGenotypeMESH: Bacterial InfectionsVirulence FactorsVirulenceEnterococcus faecalisMicrobiologyMESH : Caenorhabditis elegans03 medical and health sciencesIn vivoMESH: Anti-Bacterial AgentsMESH: Caenorhabditis elegansmedicineEscherichia coliAnimalsCaenorhabditis elegansEscherichia coli030304 developmental biologyMESH: Virulence Factors030306 microbiologylcsh:RMicrobiology/Medical Microbiology[SDV.EE.IEO] Life Sciences [q-bio]/Ecology environment/Symbiosisbiology.organism_classificationMESH : Disease Models AnimalDisease Models AnimalEnterococcuslcsh:QMESH : AnimalsMESH: Disease Models Animal[SDV.EE.IEO]Life Sciences [q-bio]/Ecology environment/SymbiosisPloS one
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Early mitochondrial dysfunction, superoxide anion production, and DNA degradation are associated with non-apoptotic death of human airway epithelial …

2002

It has been shown that bacterial exoproducts may induce airway epithelium injury. During the epithelial repair process, the respiratory epithelial cells no more establish tight junctional intercellular complexes and may be particularly susceptible to bacterial virulence factors. In this study, we analyzed the effect of Pseudomonas aeruginosa exotoxin A (ETA) at different periods of time and concentrations on 16 HBE 14o(-) human bronchial epithelial cells in culture conditions inducing a phenotype of repairing cells. ETA treatment for 24 and 48 h led to the killing of 40.0 +/- 5.7% and 79.0 +/- 1.4% of the cells, respectively, as determined by the dimethylthiazole 2,5 diphenyl tetrazolium br…

MESH: Cell DeathMESH: ADP Ribose TransferasesMESH : DNAClinical BiochemistryCellApoptosisMESH : Dose-Response Relationship DrugMitochondrion[SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractMembrane PotentialsMESH: Dose-Response Relationship Drugchemistry.chemical_compoundSuperoxidesMESH: Intracellular MembraneMESH : DNA FragmentationRespiratory systemEnzyme InhibitorsCells CulturedADP Ribose TransferasesMESH : Cell SurvivalCell DeathSuperoxideMESH: DNAMESH: BronchiCaspase InhibitorsMESH : BronchiMitochondriaMESH : Epithelial Cellsmedicine.anatomical_structureMESH: Cell SurvivalMESH: Enzyme InhibitorsMESH: Epithelial CellsMESH : ADP Ribose TransferasesIntracellularMESH: Cells CulturedPulmonary and Respiratory MedicineProgrammed cell deathCell SurvivalVirulence FactorsBacterial ToxinsExotoxinsBronchiDNA FragmentationRespiratory MucosaBiologyMicrobiologyNecrosisNasal PolypsMESH : Cells CulturedmedicineHumansMESH: DNA FragmentationMESH : Intracellular MembraneMolecular BiologyMESH : Enzyme InhibitorsMESH: HumansMESH: CaspasesDose-Response Relationship DrugMESH: ApoptosisMESH : HumansEpithelial CellsCell BiologyDNAIntracellular MembranesMESH: ExotoxinschemistryMESH: Bacterial ToxinsApoptosisMESH : ExotoxinsMESH : Cell DeathMESH : Bacterial ToxinsRespiratory epithelium[SDV.MHEP.PSR] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractMESH : CaspasesMESH : Apoptosis[ SDV.MHEP.PSR ] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tract
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Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells.

2008

International audience; The Candida albicans gpi7/gpi7 null mutant strain (Deltagpi7), which is affected in glycosylphosphatidylinositol (GPI) anchor biosynthesis, showed a reduced virulence following systemic infection of C57BL/6 mice. In vitro production of TNF-alpha, IL-6 and IL-1beta by macrophages in response to Deltagpi7 cells was significantly increased as compared to control (wild type GPI7/GPI7 and revertant gpi7/GPI7) cells; this probably contributes to the enhanced recruitment of neutrophils to the peritoneal cavity in response to Deltagpi7 cells. Survival of knockout mice for Toll-like receptor (TLR) 2 and TLR4 following intravenous injection of Deltagpi7 cells showed no signifi…

MESH: InflammationGlycosylphosphatidylinositolsNeutrophilsmedicine.medical_treatmentInterleukin-1betasourisMESH: NeutrophilsMESH: VirulenceMESH: Mice KnockoutMiceMESH: Interleukin-1betaNull cellMESH: AnimalsCandida albicansPeritoneal CavityCells CulturedMice Knockout0303 health sciencesToll-like receptorbiologyVirulenceMESH: Toll-Like Receptor 2MESH: Peritoneal CavityMESH: Toll-Like Receptor 4MESH: GlycosylphosphatidylinositolsInfectious DiseasesCytokineMESH: Survival AnalysisTumor necrosis factor alphaMESH: Fungal Proteinsprotéine de la paroi cellulaireMESH: Macrophages PeritonealMESH: Cells CulturedVirulence FactorsImmunologyMicrobiologyMicrobiologyProinflammatory cytokineFungal Proteins03 medical and health sciencesMESH: Mice Inbred C57BLmedicineAnimalsMESH: Mice030304 developmental biologyMESH: Virulence FactorsInflammation030306 microbiologyInterleukin-6Tumor Necrosis Factor-alphaMESH: Candida albicans[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologybiology.organism_classificationSurvival AnalysispathogénicitéMESH: Interleukin-6Toll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4TLR2GlycosylphosphatidylinositolMESH: Gene DeletionMESH: Tumor Necrosis Factor-alphaTLR4Macrophages Peritonealcandida albicansimmunitéGene Deletion
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