Escherichia coli HS strain:HS
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA13959 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Avian pathogenic Escherichia coli strains frequently cause extra-intestinal infections and are responsible for significant economic losses in the poultry industry worldwide. APEC isolates are closely related to human extraintestinal pathogenic E.coli strains and may also act as pathogens for humans. In this work, three type VI secretion systems were deleted to analyze which pathogenicity characteristics would change in the mutants, compared to wild type strain (SEPT 362).
2010-09-10 | GSE21893 | GEO
Project description:Urinary tract infections (UTIs) are a very common bacterial infectious disease in humans, and uropathogenic Escherichia coli (UPEC) are the most frequent cause of UTIs. During infection, UPEC must cope with a variety of stressful conditions in the urinary tract. Here, we demonstrated that the small RNA (sRNA) RyfA of UPEC strains was required for resistance to oxidative and osmotic stresses. Inactivation of ryfA in UPEC strain CFT073 decreased urinary tract colonization in CBA/J mice and the ryfA mutant also had reduced production of type 1 and P fimbriae, which are known to be important for UTI. Transcriptomic analysis of the ryfA mutant showed changes in expression of genes associated with general stress responses, metabolism, biofilm formation and genes coding for cell surface proteins. Furthermore, loss of ryfA also reduced UPEC survival in human macrophages. Thus, ryfA plays a key regulatory role in UPEC adaptation to stress, that contributes to UTI and survival in macrophages.
2021-06-23 | GSE157450 | GEO
Project description:Escherichia coli, one of the most abundant bacterial species in the human gut microbiota, has developed a mutualistic relationship with its host, regulating immunological responses. In contrast, enterotoxigenic E. coli (ETEC), one of the main etiologic agents of diarrheal morbidity and mortality in children under the age of five in developing countries, has developed mechanisms to reduce the immune-activator effect to carry out a successful infection. Following infection, the host cell initiates the shutting-off of protein synthesis and stress granule (SG) assembly. This is mostly mediated by the phosphorylation of translation initiator factor 2? (eIF2?). We therefore evaluated the ability of a non-pathogenic E. coli strain (E. coli HS) and an ETEC strain (ETEC 1766a) to induce stress granule assembly, even in response to exogenous stresses. In this work, we found that infection with E. coli HS or ETEC 1766a prevents SG assembly in Caco-2 cells treated with sodium arsenite (Ars) after infection. We also show that this effect occurs through an eIF2? phosphorylation (eIF2?-P)-dependent mechanism. Understanding how bacteria counters host stress responses will lay the groundwork for new therapeutic strategies to bolster host cell immune defenses against these pathogens.
| S-EPMC7822485 | biostudies-literature
Project description:These E. coli strains were grown with various signaling molecules and the expression profiles were determined. Keywords: addition of quorum and host hormone signals
2007-09-20 | GSE7439 | GEO
Project description:Identification of transcriptional pathways associated with enviromental modification
| PRJNA237645 | ENA
Project description:Mucosal surfaces provide ideal living conditions for the normal flora but paradoxically, they also serve as attack sites for numerous bacterial pathogens that cause extensive morbidity and mortality. Understanding this dichotomy is critical for efforts to selectively target and remove pathogens without disturbing the commensal flora or its protective effects. The complex nature of disease predicts that virulence is multifaceted and that pathogens need multiple virulence factors to initiate tissue attack, disrupt immune homeostasis and create symptoms and pathology. The urinary tract supports ABU; a commensal-like state, which has been shown to prevent super-infection with more virulent strains. To reproduce this protective effect, we have established a protocol to create ABU, by inoculation with the ABU strain E. coli 83972. The therapeutic efficacy and safety of this procedure has been documented in placebo-controlled studies in patients with incomplete bladder voiding. Genome sequencing of E. coli 83972 has revealed a general “loss of virulence” phenotype, which includes fimbrial genes. E. coli 83972 lacks functional P or type 1 fimbriae, due to attenuating point mutations in the papG adhesin gene and a large, inactivating deletion in the fim gene cluster. Both fimbrial types have been proposed to enhance bacterial persistence in the urinary tract. In an attempt to increase the efficiency of E. coli 83972 inoculation and extend its use to include UTI-prone patients with complete bladder voiding, we restored P- and type 1-fimbrial expression and addressed how fimbriae affect the gene expression in inoculated human hosts.
2019-03-20 | GSE128557 | GEO
Project description:Avian pathogenic Escherichia coli strains frequently cause extra-intestinal infections and are responsible for significant economic losses in the poultry industry worldwide. APEC isolates are closely related to human extraintestinal pathogenic E.coli strains and may also act as pathogens for humans. In this work, three type VI secretion systems were deleted to analyze which pathogenicity characteristics would change in the mutants, compared to wild type strain (SEPT 362). Four Avian Pathogenic Escherichia coli strains (one wild type and three deleted mutants) were grown at 37°C in Dulbecco´s Modified Eagle´s Media (DMEM) media until reach O.D 600 = 0.8, for RNA extraction and hybridization on Affymatrix microarrays.
2010-09-09 | E-GEOD-21893 | biostudies-arrayexpress
Project description:The complex reservoir of metabolite-producing bacteria in the gastrointestinal tract contributes tremendously to human health and disease. Bacterial composition, and by extension gut metabolomic composition, is undoubtably influenced by the use of modern antibiotics. Herein, we demonstrate that polymyxin B, a last resort antibiotic used for chronic multidrug resistant infections infections, influences the production of the genotoxic metabolite colibactin from adherent-invasive Escherichia coli (AIEC) NC101. Colibactin can augment colorectal cancer (CRC) through DNA double stranded breaks and interstrand crosslinks. While the structure and biosynthesis of colibactin has been elucidated, chemical-induced regulation of its biosynthetic gene cluster and subsequent production of the genotoxin by pathogenic E. coli are largely unexplored. This research highlights the regulation of the colibactin-producing biosynthetic gene cluster under polymyxin stress. Using a multi-omic approach, we have identified that polymyxin stress enhances the abundance of colibactin biosynthesis proteins (Clb’s) in multiple pks+ E. coli strains, including pro-carcinogenic AIEC: NC101, the probiotic strain: E. coli Nissle 1917, and the antibiotic testing strain: E. coli ATCC 25922. Expression analysis via qPCR revealed that increased transcription of clb genes likely contributes to elevated Clb protein levels in NC101. Enhanced production of Clb’s by NC101 under polymyxin stress matched an increased production of the colibactin prodrug motif, a proxy for the mature genotoxic metabolite. Furthermore, E. coli with heightened tolerance for polymyxin antibiotics induced greater DNA damage, assessed by quantification of γH2AX staining in cultured intestinal epithelial cells. This study establishes a key link between the polymyxin B stress response and colibactin production in pks+ E. coli. Ultimately, our findings will inform future studies investigating colibactin regulation, the microbial response to antibiotics in the gut, and the ability of seemingly innocuous commensal microbes to induce host disease.
2021-07-15 | PXD025088 | Pride