Escherichia coli HS strain:HS
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA13959 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR9418130.fastq.gz | Fastqsanger.gz | |||
| SRR9418131.fastq.gz | Fastqsanger.gz | |||
| SRR9418132.fastq.gz | Fastqsanger.gz | |||
| SRR9418127.fastq.gz | Fastqsanger.gz |
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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 2α (eIF2α). 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 eIF2α phosphorylation (eIF2α-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.
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Project description:Gene content comparison of control C.j. strain 11168 which colonizes and causes disease in a murine model versus strain NW which colonizes but does not elicit disease symptomology in the mouse model. Keywords: DNA/DNA comparison
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Project description:Gene content comparison of control C.j. strain 11168 which colonizes and causes disease in a murine model versus strain NW which colonizes but does not elicit disease symptomology in the mouse model. Keywords: DNA/DNA comparison Two genome comparison of disease strain versus non disease strain of C.j., Biological replicates - 2, independently grown and harvested, Technical replicates 2, also independent, 3 ORF replicates per array.
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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.
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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.
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