about
Flagellin-dependent and -independent inflammatory responses following infection by enteropathogenic Escherichia coli and Citrobacter rodentiumSalmonella pathogenicity island 2 is expressed prior to penetrating the intestine.SopD2 is a novel type III secreted effector of Salmonella typhimurium that targets late endocytic compartments upon delivery into host cellsA novel secretion pathway of Salmonella enterica acts as an antivirulence modulator during salmonellosisDissemination of invasive Salmonella via bacterial-induced extrusion of mucosal epithelia.Muc2 protects against lethal infectious colitis by disassociating pathogenic and commensal bacteria from the colonic mucosa.Epithelial p38alpha controls immune cell recruitment in the colonic mucosa.Modulation of host cytoskeleton function by the enteropathogenic Escherichia coli and Citrobacter rodentium effector protein EspGIndispensable functions of ABL and PDGF receptor kinases in epithelial adherence of attaching/effacing pathogens under physiological conditions.Critical role for signal transducer and activator of transcription factor 6 in mediating intestinal muscle hypercontractility and worm expulsion in Trichinella spiralis-infected miceCloning vectors and fluorescent proteins can significantly inhibit Salmonella enterica virulence in both epithelial cells and macrophages: implications for bacterial pathogenesis studies.Clearance of Citrobacter rodentium requires B cells but not secretory immunoglobulin A (IgA) or IgM antibodies.Regulated virulence controls the ability of a pathogen to compete with the gut microbiota.Toll-like receptor 4 contributes to colitis development but not to host defense during Citrobacter rodentium infection in mice.The Toll-interleukin-1 receptor member SIGIRR regulates colonic epithelial homeostasis, inflammation, and tumorigenesis.Nramp1 expression by dendritic cells modulates inflammatory responses during Salmonella Typhimurium infection.Antibiotic treatment alters the colonic mucus layer and predisposes the host to exacerbated Citrobacter rodentium-induced colitis.Requirement of epithelial integrin-linked kinase for facilitation of Citrobacter rodentium-induced colitis.Host susceptibility to the attaching and effacing bacterial pathogen Citrobacter rodentiumTACI deficiency enhances antibody avidity and clearance of an intestinal pathogenAttaching and effacing bacterial effector NleC suppresses epithelial inflammatory responses by inhibiting NF-κB and p38 mitogen-activated protein kinase activation.A novel mouse model of Campylobacter jejuni gastroenteritis reveals key pro-inflammatory and tissue protective roles for Toll-like receptor signaling during infection.Aggregation via the red, dry, and rough morphotype is not a virulence adaptation in Salmonella enterica serovar Typhimurium.Active vitamin D (1,25-dihydroxyvitamin D3) increases host susceptibility to Citrobacter rodentium by suppressing mucosal Th17 responses.Absence of stearoyl-CoA desaturase-1 does not promote DSS-induced acute colitis.SseK1 and SseK2 are novel translocated proteins of Salmonella enterica serovar typhimurium.Innate host responses to enteric bacterial pathogens: a balancing act between resistance and tolerance.Enteropathogenic Escherichia coli infection induces expression of the early growth response factor by activating mitogen-activated protein kinase cascades in epithelial cells.Citrobacter rodentium infection induces MyD88-dependent formation of ubiquitinated protein aggregates in the intestinal epithelium.The single IgG IL-1-related receptor controls TLR responses in differentiated human intestinal epithelial cellsCitrobacter rodentium infection causes both mitochondrial dysfunction and intestinal epithelial barrier disruption in vivo: role of mitochondrial associated protein (Map).Salmonella infection of gallbladder epithelial cells drives local inflammation and injury in a model of acute typhoid fever.Loss of single immunoglobulin interlukin-1 receptor-related molecule leads to enhanced colonic polyposis in Apc(min) mice.Salmonella enterica serovar Typhimurium pathogenicity island 2 is necessary for complete virulence in a mouse model of infectious enterocolitis.Intestinal epithelium-specific MyD88 signaling impacts host susceptibility to infectious colitis by promoting protective goblet cell and antimicrobial responses.CD4+ T cells drive goblet cell depletion during Citrobacter rodentium infection.SseA is required for translocation of Salmonella pathogenicity island-2 effectors into host cells.Vasoactive intestinal peptide ameliorates intestinal barrier disruption associated with Citrobacter rodentium-induced colitis.Colonic microbiota alters host susceptibility to infectious colitis by modulating inflammation, redox status, and ion transporter gene expression.Interleukin-11 reduces TLR4-induced colitis in TLR2-deficient mice and restores intestinal STAT3 signaling.
P50
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P50
description
hulumtues
@sq
onderzoeker
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researcher
@en
հետազոտող
@hy
name
Bruce A. Vallance
@ast
Bruce A. Vallance
@en
Bruce A. Vallance
@es
Bruce A. Vallance
@sl
type
label
Bruce A. Vallance
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Bruce A. Vallance
@en
Bruce A. Vallance
@es
Bruce A. Vallance
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Bruce Vallance
@en
prefLabel
Bruce A. Vallance
@ast
Bruce A. Vallance
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Bruce A. Vallance
@es
Bruce A. Vallance
@sl
P106
P1153
7003803048
P21
P31
P496
0000-0003-1345-6747