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TraDIS in UPEC

ABSTRACT: The fitness landscape of UPEC during UTIs

PROVIDER: PRJEB41961 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	ERR5059490.fastq.gz	Fastqsanger.gz
	ERR5059500.fastq.gz	Fastqsanger.gz
	ERR5059510.fastq.gz	Fastqsanger.gz
	ERR5059520.fastq.gz	Fastqsanger.gz
	ERR5059491.fastq.gz	Fastqsanger.gz

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Genetically diverse uropathogenic Escherichia coli adopt a common transcriptional program in patients with urinary tract infections

Project description:Uropathogenic Escherichia coli (UPEC) is the major causative agent of uncomplicated urinary tract infections (UTIs). A common virulence genotype of UPEC strains responsible for UTIs is yet to be defined, due to the large variation of virulence factors observed in UPEC strains. We hypothesized that studying UPEC functional responses in patients might reveal universal UPEC features that enable pathogenesis. Here we identify a transcriptional program shared by genetically diverse UPEC strains isolated from 14 patients during uncomplicated UTIs. Strikingly, this in vivo gene expression program is marked by upregulation of translational machinery, providing a mechanism for the rapid growth within the host. Our analysis indicates that switching to a more specialized catabolism and scavenging lifestyle in the host allows for the increased translational output. Our study identifies a common transcriptional program underlying UTIs and illuminates the molecular underpinnings that likely facilitate the fast growth rate of UPEC in infected patients.

2019-10-29 | GSE128997 | GEO

CD137L+Macrophage Resolves Acute Cystitis Induced by UPEC Infection through Regulatory T Cells Activation

Project description:Urinary tract infections (UTIs) typically evoke prompt and vigorous innate immune responses in bladder, but the specific mechanisms that resolute acute inflammation remain unclear. In this study, single-cell RNA sequencing and analysis of immune cells from the bladder at early stage of uropathogenic Escherichia coli (UPEC) infection was performed. The increased hyperactivated CD137L+macrophage response and decreased immunosuppressive Treg cells are elucidated in the bladder microenvironment of UPEC infection. Conditional depletion of CD137L in macrophage aggravates inflammatory reaction, bacterial load and urothelium destruction. Deletion of Treg cells also aggravated inflammation while promoting urothelial injury after UPEC infection. Additionally, Treg cells were increased in infected bladder which can be reversed by a myeloid-CD137L deletion. We thought activation of Treg cells by CD137L+macrophage is a key mechanism for suppressing acute inflammatory reaction after UPEC infection. The present study provided new insights into the functions of myeloid-CD137L dependent Treg cells in the immune response to UPEC infection.

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The RyfA small RNA serves as a master regulator of stress responses and virulence in uropathogenic Escherichia coli

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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Expression data in UPEC cystitis in female CBA mice

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RNA sequencing analysis of bladder tissue from CFT073-infected C57B/6J mice with or without treatments of D-xyl@epsilonPLCDs and epsilonPLCDs

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Using a Zebrafish Model to Identify Cellular Responses to Uropathogenic E. coli Bacteremia

Project description:Urinary tract infections (UTIs) are the second most common infections encountered in the pediatric population, second only to respiratory tract infections. UTIs are also a major cause of morbidity and mortality. UTIs can often ascend causing infection in the upper urinary tract or even progress to bacteremia or urosepsis. Urosepsis accounts for 10-30% of septic shock cases and Uropathogenic E.coli (UPEC) is responsible for almost 75% of cases. Therefore, increased understanding of the effects of urosepsis at the cellular and organ specific level will provide the foundation for improvements in clinical care.

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Expression data in UPEC cystitis in female CBA mice

Project description:Data defines for the first time a whole bladder transcriptome of UPEC cystitis in female CBA mice using genome-wide expression profiling to map early host response pathways stemming from UPEC colonization We used microarrays to detail the global programme of gene expression in UPEC UTI in mice Whole mouse bladder collected at 2h following transurethral infection for RNA extraction and hybridization on Affymetrix microarrays. Non-pooled samples were used, with one array per mouse to expand power of expression profiles. Control mice received only PBS as a mock infection. Group sizes were five mice per group, and therefore five arrays were used per group.

2011-12-28 | E-GEOD-33210 | biostudies-arrayexpress

Expression data in UPEC cystitis in female C57BL/6 mice

Project description:Data defines for the first time a whole bladder transcriptome of UPEC cystitis in female C57BL/6 mice using genome-wide expression profiling to map early host response pathways stemming from UPEC colonization We used microarrays to detail the global programme of gene expression in UPEC UTI in mice Whole mouse bladder collected at 2h following transurethral infection for RNA extraction and hybridization on Affymetrix microarrays. Non-pooled samples were used, with one array per mouse to expand power of expression profiles. Control mice received only PBS as a mock infection. Group sizes were five mice per group, and therefore five arrays were used per group.

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