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Dissecting virulence: systematic and functional analyses of a pathogenicity island.
TLDR
This work systematically mutagenized all 41 CR LEE genes and functionally characterized these mutants in vitro and in a murine infection model, identifying 33 virulence factors, including two virulence regulators and a hierarchical switch for type III secretion.
The adaptor Act1 is required for interleukin 17–dependent signaling associated with autoimmune and inflammatory disease
TLDR
The data show that Act1 is essential in IL-17-dependent signaling in autoimmune and inflammatory disease and was associated with much less inflammatory disease in vivo in both autoimmune encephalomyelitis and dextran sodium sulfate–induced colitis.
Salmonella effectors within a single pathogenicity island are differentially expressed and translocated by separate type III secretion systems
TLDR
A functional and regulatory cross‐talk between three chromosomal PAIs, SPI‐1, SPI-2 and SPI‐5, has significant implications for the evolution and role of PAIs in bacterial pathogenesis.
Dissemination of invasive Salmonella via bacterial-induced extrusion of mucosal epithelia
TLDR
It is demonstrated that a subpopulation of Salmonella hyperreplicating in the cytosol of epithelial cells serves as a reservoir for dissemination and provides a mechanistic explanation for the mucosal inflammation that is triggered duringSalmonella infection of the gastrointestinal and biliary tracts.
Regulated Virulence Controls the Ability of a Pathogen to Compete with the Gut Microbiota
TLDR
It is shown that germ-free animals are unable to eradicate Citrobacter rodentium, a model for human infections with attaching and effacing bacteria, and pathogen colonization is controlled by bacterial virulence and through competition with metabolically related commensals.
Locus of Enterocyte Effacement from Citrobacter rodentium: Sequence Analysis and Evidence for Horizontal Transfer among Attaching and Effacing Pathogens
TLDR
The results indicate that the full DNA sequence of C.rodentium LEE has been acquired by C. rodentium and A/E E.coli strains independently during evolution.
Citrobacter rodentium translocated intimin receptor (Tir) is an essential virulence factor needed for actin condensation, intestinal colonization and colonic hyperplasia in mice
TLDR
It is shown that Tir, but not its tyrosine phosphorylation, is essential for C. rodentium to colonize the large bowel and induce attaching/effacing (A/E) lesions and colonic hyperplasia in mice, and that both EPEC Tir and EHEC Tir can substitute for Citrobacter Tir for these activities in vivo.
Exploitation of host cells by enteropathogenic Escherichia coli.
TLDR
Future studies of A/E pathogens in animal models should provide further insights into how EPEC exploits not only epithelial cells but other host cells, including those of the immune system, to cause diarrheal disease.
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