Bruce A. Vallance

Mice lacking T and B lymphocytes develop transient colitis and crypt hyperplasia yet suffer impaired bacterial clearance during Citrobacter rodentium infection.

Salmonella effectors within a single pathogenicity island are differentially expressed and translocated by separate type III secretion systems.

Modulation of inducible nitric oxide synthase expression by the attaching and effacing bacterial pathogen citrobacter rodentium in infected mice.

Host-pathogen interactions: Host resistance factor Nramp1 up-regulates the expression of Salmonella pathogenicity island-2 virulence genes.

Enteropathogenic and enterohemorrhagic Escherichia coli infections: emerging themes in pathogenesis and prevention.

SopD2 is a novel type III secreted effector of Salmonella typhimurium that targets late endocytic compartments upon delivery into host cells.

Citrobacter rodentium translocated intimin receptor (Tir) is an essential virulence factor needed for actin condensation, intestinal colonization and colonic hyperplasia in mice.

Host susceptibility to the attaching and effacing bacterial pathogen Citrobacter rodentium.

SseA is required for translocation of Salmonella pathogenicity island-2 effectors into host cells.

Salmonella type III effectors PipB and PipB2 are targeted to detergent-resistant microdomains on internal host cell membranes.

Current progress in enteropathogenic and enterohemorrhagic Escherichia coli vaccines.

Dissecting virulence: systematic and functional analyses of a pathogenicity island.

Toll-like receptor 4 dependence of innate and adaptive immunity to Salmonella: importance of the Kupffer cell network.

Clearance of Citrobacter rodentium requires B cells but not secretory immunoglobulin A (IgA) or IgM antibodies.

Relative contributions of NOS isoforms during experimental colitis: endothelial-derived NOS maintains mucosal integrity.

SseK1 and SseK2 are novel translocated proteins of Salmonella enterica serovar typhimurium.

Myenteric plexus injury and apoptosis in experimental colitis.

TGF-beta1 gene transfer to the mouse colon leads to intestinal fibrosis.

Modulation of host cytoskeleton function by the enteropathogenic Escherichia coli and Citrobacter rodentium effector protein EspG.

Salmonella enterica serovar Typhimurium pathogenicity island 2 is necessary for complete virulence in a mouse model of infectious enterocolitis.

Cloning vectors and fluorescent proteins can significantly inhibit Salmonella enterica virulence in both epithelial cells and macrophages: implications for bacterial pathogenesis studies.

Salmonella pathogenicity island 2 is expressed prior to penetrating the intestine.

Noradrenergic and cholinergic neural pathways mediate stress-induced reactivation of colitis in the rat.

Toll-like receptor 4 contributes to colitis development but not to host defense during Citrobacter rodentium infection in mice.

Citrobacter rodentium infection causes both mitochondrial dysfunction and intestinal epithelial barrier disruption in vivo: role of mitochondrial associated protein (Map).

Genetic profiling of dendritic cells exposed to live- or ultraviolet-irradiated Chlamydia muridarum reveals marked differences in CXC chemokine profiles.

IL-4 gene transfer to the small bowel serosa leads to intestinal inflammation and smooth muscle hyperresponsiveness.

The Toll-interleukin-1 receptor member SIGIRR regulates colonic epithelial homeostasis, inflammation, and tumorigenesis.

Toll-like receptor 2 plays a critical role in maintaining mucosal integrity during Citrobacter rodentium-induced colitis.

Modulation of intestinal goblet cell function during infection by an attaching and effacing bacterial pathogen.

Role of M-CSF-dependent macrophages in colitis is driven by the nature of the inflammatory stimulus.

Flagellin-dependent and -independent inflammatory responses following infection by enteropathogenic Escherichia coli and Citrobacter rodentium.

Chronic enteric salmonella infection in mice leads to severe and persistent intestinal fibrosis.

A novel secretion pathway of Salmonella enterica acts as an antivirulence modulator during salmonellosis.

Nramp1 expression by dendritic cells modulates inflammatory responses during Salmonella Typhimurium infection.

Nramp1 drives an accelerated inflammatory response during Salmonella-induced colitis in mice.

Intestinal microbiota are transiently altered during Salmonella-induced gastroenteritis.

Absence of stearoyl-CoA desaturase-1 does not promote DSS-induced acute colitis.

Salmonella infection of gallbladder epithelial cells drives local inflammation and injury in a model of acute typhoid fever.

The single IgG IL-1-related receptor controls TLR responses in differentiated human intestinal epithelial cells.

Control of intestinal homeostasis, colitis, and colitis-associated colorectal cancer by the inflammatory caspases.

The pathogenic E. coli type III effector EspZ interacts with host CD98 and facilitates host cell prosurvival signalling.

Loss of single immunoglobulin interlukin-1 receptor-related molecule leads to enhanced colonic polyposis in Apc(min) mice.

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.

Interleukin-11 reduces TLR4-induced colitis in TLR2-deficient mice and restores intestinal STAT3 signaling.

Dissemination of invasive Salmonella via bacterial-induced extrusion of mucosal epithelia.

Citrobacter rodentium infection induces MyD88-dependent formation of ubiquitinated protein aggregates in the intestinal epithelium.

Attaching and effacing bacterial effector NleC suppresses epithelial inflammatory responses by inhibiting NF-κB and p38 mitogen-activated protein kinase activation.

Innate host responses to enteric bacterial pathogens: a balancing act between resistance and tolerance.

Regulated virulence controls the ability of a pathogen to compete with the gut microbiota.

MyD88 signaling promotes both mucosal homeostatic and fibrotic responses during Salmonella-induced colitis.

Active vitamin D (1,25-dihydroxyvitamin D3) increases host susceptibility to Citrobacter rodentium by suppressing mucosal Th17 responses.

Resistin-like Molecule α Promotes Pathogenic Th17 Cell Responses and Bacterial-Induced Intestinal Inflammation.