about
Structural basis for the reversible activation of a Rho protein by the bacterial toxin SopE.Phages and the evolution of bacterial pathogens: from genomic rearrangements to lysogenic conversionNADPH oxidase deficient mice develop colitis and bacteremia upon infection with normally avirulent, TTSS-1- and TTSS-2-deficient Salmonella TyphimuriumSalmonella transiently reside in luminal neutrophils in the inflamed gutAn NK Cell Perforin Response Elicited via IL-18 Controls Mucosal Inflammation Kinetics during Salmonella Gut InfectionA simple screen to identify promoters conferring high levels of phenotypic noiseThe microbiota mediates pathogen clearance from the gut lumen after non-typhoidal Salmonella diarrheaBistable expression of virulence genes in salmonella leads to the formation of an antibiotic-tolerant subpopulationCecum lymph node dendritic cells harbor slow-growing bacteria phenotypically tolerant to antibiotic treatmentClostridium difficile toxin CDT induces formation of microtubule-based protrusions and increases adherence of bacteriaGranulocytes impose a tight bottleneck upon the gut luminal pathogen population during Salmonella typhimurium colitisStromal IFN-γR-signaling modulates goblet cell function during Salmonella Typhimurium infectionSalmonella enterica serovar typhimurium exploits inflammation to compete with the intestinal microbiotaNear surface swimming of Salmonella Typhimurium explains target-site selection and cooperative invasionThe cost of virulence: retarded growth of Salmonella Typhimurium cells expressing type III secretion system 1Salmonella effectors within a single pathogenicity island are differentially expressed and translocated by separate type III secretion systemsSalmonella-induced mucosal lectin RegIIIβ kills competing gut microbiotaA Genome-Wide siRNA Screen Implicates Spire1/2 in SipA-Driven Salmonella Typhimurium Host Cell InvasionIL-17A/F-signaling does not contribute to the initial phase of mucosal inflammation triggered by S. TyphimuriumReal-time imaging of type III secretion: Salmonella SipA injection into host cells.Hierarchical effector protein transport by the Salmonella Typhimurium SPI-1 type III secretion system.S. typhimurium encodes an activator of Rho GTPases that induces membrane ruffling and nuclear responses in host cells.Like will to like: abundances of closely related species can predict susceptibility to intestinal colonization by pathogenic and commensal bacteria.Enhanced CellClassifier: a multi-class classification tool for microscopy imagesCaspase-1 activation via Rho GTPases: a common theme in mucosal infections?Salmonella pathogenicity island 2-mediated overexpression of chimeric SspH2 proteins for simultaneous induction of antigen-specific CD4 and CD8 T cells.Bacterial colitis increases susceptibility to oral prion disease.In macrophages, caspase-1 activation by SopE and the type III secretion system-1 of S. typhimurium can proceed in the absence of flagellin.Comparison of Salmonella enterica serovar Typhimurium colitis in germfree mice and mice pretreated with streptomycin.Salmonella typhimurium encodes a putative iron transport system within the centisome 63 pathogenicity island.Pilot study to evaluate microarray hybridization as a tool for Salmonella enterica serovar Typhimurium strain differentiation.Absence of poly(ADP-ribose) polymerase 1 delays the onset of Salmonella enterica serovar Typhimurium-induced gut inflammationMechanisms controlling pathogen colonization of the gut.Virulence of broad- and narrow-host-range Salmonella enterica serovars in the streptomycin-pretreated mouse model.Live attenuated S. Typhimurium vaccine with improved safety in immuno-compromised mice.Salmonella enterica serovar Typhimurium binds to HeLa cells via Fim-mediated reversible adhesion and irreversible type three secretion system 1-mediated docking.Amino acids of the bacterial toxin SopE involved in G nucleotide exchange on Cdc42.Characterization of effector proteins translocated via the SPI1 type III secretion system of Salmonella typhimurium.TLR5 signaling stimulates the innate production of IL-17 and IL-22 by CD3(neg)CD127+ immune cells in spleen and mucosa.Flagella and chemotaxis are required for efficient induction of Salmonella enterica serovar Typhimurium colitis in streptomycin-pretreated mice.
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P50
description
researcher, ORCID id # 0000-0002-9892-6420
@en
wetenschapper
@nl
name
Wolf-Dietrich Hardt
@ast
Wolf-Dietrich Hardt
@en
Wolf-Dietrich Hardt
@es
Wolf-Dietrich Hardt
@nl
type
label
Wolf-Dietrich Hardt
@ast
Wolf-Dietrich Hardt
@en
Wolf-Dietrich Hardt
@es
Wolf-Dietrich Hardt
@nl
prefLabel
Wolf-Dietrich Hardt
@ast
Wolf-Dietrich Hardt
@en
Wolf-Dietrich Hardt
@es
Wolf-Dietrich Hardt
@nl
P106
P108
P21
P31
P496
0000-0002-9892-6420