about
Role of the Yersinia pestis yersiniabactin iron acquisition system in the incidence of flea-borne plagueNew insights into how Yersinia pestis adapts to its mammalian host during bubonic plagueProtection against Yersinia pseudotuberculosis infection conferred by a Lactococcus lactis mucosal delivery vector secreting LcrV.Transit through the flea vector induces a pretransmission innate immunity resistance phenotype in Yersinia pestisThe superantigen gene ypm is located in an unstable chromosomal locus of Yersinia pseudotuberculosisEfficacy of ciprofloxacin-gentamicin combination therapy in murine bubonic plague.Functional and structural analysis of HicA3-HicB3, a novel toxin-antitoxin system of Yersinia pestisTLR5 signaling stimulates the innate production of IL-17 and IL-22 by CD3(neg)CD127+ immune cells in spleen and mucosa.Adaptive response of Yersinia pestis to extracellular effectors of innate immunity during bubonic plague.Yersinia pestis YopJ suppresses tumor necrosis factor alpha induction and contributes to apoptosis of immune cells in the lymph node but is not required for virulence in a rat model of bubonic plagueSuperantigenic Yersinia pseudotuberculosis induces the expression of granzymes and perforin by CD4+ T cellsEvaluation of the Role of the opgGH Operon in Yersinia pseudotuberculosis and Its Deletion during the Emergence of Yersinia pestisCharacterization of the protective immune response to Yersinia pseudotuberculosis infection in mice vaccinated with an LcrV-secreting strain of Lactococcus lactis.Drug design from the cryptic inhibitor envelope.Analysis of Yersinia pestis gene expression in the flea vector.The Yersinia pestis caf1M1A1 fimbrial capsule operon promotes transmission by flea bite in a mouse model of bubonic plagueFlea-borne transmission model to evaluate vaccine efficacy against naturally acquired bubonic plague.Evaluation of the role of constitutive isocitrate lyase activity in Yersinia pestis infection of the flea vector and mammalian host.Curative Treatment of Severe Gram-Negative Bacterial Infections by a New Class of Antibiotics Targeting LpxC.Inheritance of the lysozyme inhibitor Ivy was an important evolutionary step by Yersinia pestis to avoid the host innate immune response.High susceptibility of MDR and XDR Gram-negative pathogens to biphenyl-diacetylene-based difluoromethyl-allo-threonyl-hydroxamate LpxC inhibitors.Genes encoding specific nickel transport systems flank the chromosomal urease locus of pathogenic yersiniae.Yersinia pestis requires the 2-component regulatory system OmpR-EnvZ to resist innate immunity during the early and late stages of plague.Autophagosomes can support Yersinia pseudotuberculosis replication in macrophages.Poor vector competence of fleas and the evolution of hypervirulence in Yersinia pestis.The pmrF polymyxin-resistance operon of Yersinia pseudotuberculosis is upregulated by the PhoP-PhoQ two-component system but not by PmrA-PmrB, and is not required for virulence.The Yersinia pseudotuberculosis Yut protein, a new type of urea transporter homologous to eukaryotic channels and functionally interchangeable in vitro with the Helicobacter pylori UreI protein.Body lice, yersinia pestis orientalis, and black deathTranscriptomic studies and assessment of Yersinia pestis reference genes in various conditionsTo block or not to block: The adaptive manipulation of plague transmission.A refined model of how Yersinia pestis produces a transmissible infection in its flea vectorNutrient depletion may trigger the Yersinia pestis OmpR-EnvZ regulatory system to promote flea-borne plague transmissionPolymorphism in the Yersinia LcrV Antigen Enables Immune Escape From the Protection Conferred by an LcrV-Secreting Lactococcus Lactis in a Pseudotuberculosis Mouse Model
P50
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P50
description
hulumtues
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հետազոտող
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name
Florent Sebbane
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Florent Sebbane
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Florent Sebbane
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Florent Sebbane
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Florent Sebbane
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Florent Sebbane
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Florent Sebbane
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Florent Sebbane
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Florent Sebbane
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Florent Sebbane
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Florent Sebbane
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Florent Sebbane
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Florent Sebbane
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Florent Sebbane
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P21
P2798
P31
P496
0000-0003-3811-9691