Project description:Transcriptional profiles of uropathogenic Escherichia coli CFT073 exposed to cranberry-derived proanthocyanidins (PACs) were determined. Our results indicate that bacteria grown on media supplemented with PACs were iron-deprived. To our knowledge, this is the first time that PACs have been shown to induce a state of iron-limitation in this bacterium.
Project description:Transcriptional profiles of uropathogenic Escherichia coli CFT073 exposed to cranberry-derived proanthocyanidins (PACs) were determined. Our results indicate that bacteria grown on media supplemented with PACs were iron-deprived. To our knowledge, this is the first time that PACs have been shown to induce a state of iron-limitation in this bacterium. Cultures of E. coli CFT073 were streaked onto LB agar plates and incubated (37°C, 24 h). A single colony was inoculated into 150 mL of LB broth. Three inoculated flasks contained LB broth alone (controls), and three inoculated flasks were supplemented with cranberry PACs (100 µg/mL). After incubation (37°C, 5 h, 200 rpm to mid-log growth phase), bacteria were harvested for RNA extraction.
Project description:The purpose of this study is to determine whether the presence of pathogenic Escherichia coli in colon is associated with psychiatric disorders.
Project description:Urinary tract infections (UTIs) constitute a highly relevant model of microbial adaptation, in which the contrasting effects of pathogens and commensals on host tissues are clearly displayed. While virulent Escherichia coli cause severe, potentially life-threatening disease by breaking the inertia of the mucosal barrier and infecting the kidneys, the most common outcome of bacteriuria is an asymptomatic carrier state resembling commensalism at other mucosal sites. It remains unclear if the lack of destructive inflammation merely reflects low virulence or if carrier strains actively inhibit disease associated responses in the host. To address this question, we examined the effects of asymptomatic bacterial carriage on host gene expression. A498 cell line has been validated as a model of uropathogenic E. coli infection; the cells express functional receptors for bacterial virulence ligands and the response to virulent strains reflects human UTI. The cells were infected with asymptomatic and pathogenic E. coli in vitro, and harvested RNA was subjected to whole genome transcriptome analysis.
Project description:We previously determined that loss of respiratory quinol oxidase cytochrome bd disrupts biofilm formation in uropathogenic Escherichia coli (UPEC). In this study, we extracted and interrogated the outer membrane and extracellular matrix of colony biofilms formed by UPEC isolate UTI89 and an isogenic mutant lacking cytochrome bd (∆cydAB).
Project description:Despite the characterization of many aetiologic genetic changes. The specific causative factors in the development of sporadic colorectal cancer remain unclear. This study was performed to detect the possible role of Enteropathogenic Escherichia coli (EPEC) in developing colorectal carcinoma.
Project description:Escherichia coli release Extracellular Vesicles (EVs) which carry diverse molecular cargo. Pathogenic E.coli EVs contain virulence factors which assist during infection in the host in different mechanisms.The RNA cargo of E.coli EVs has not been assessed in their effect in the host. We used microarray data to asses and compare the global response of bladder cells to EV-RNA from pathogenic E.coli (Uropathogenic UPEC 536) and non-pathogenic E. coli (probiotic Nissle 1917)
Project description:Here we dissected a regulatory network directed by the conserved iron homeostasis regulator, Ferric Uptake Regulator (Fur), in uropathogenic E. coli strain CFT073. Comparing anaerobic genome-scale Fur DNA binding, with Fur dependent transcript expression and protein levels of the uropathogen to that of commensal E. coli K-12 strain MG1655, showed that the Fur regulon of the core genome is conserved but also includes genes within the pathogenicity/genetic islands. Unexpectedly, regulons indicative of amino acid limitation and the general stress response were also indirectly activated in the uropathogen fur mutant, suggesting that induction of the Fur regulon increases amino acid demand. Using RpoS levels as a proxy, addition of amino acids mitigated the stress. In addition, iron chelation increased RpoS to the same levels as in the fur mutant. The increased amino acid demand of the fur mutant or iron chelated cells was exacerbated by aerobic conditions, which could be partly explained by the O 2 -dependent synthesis of the siderophore aerobactin, encoded within a pathogenicity island. Taken together, this data suggest in the iron-poor environment of the urinary tract, amino acid availability could play a role in the proliferation of this uropathogen, particularly if there is sufficient O 2 to produce aerobactin.
