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Functional analysis of the uropathogenic Escherichia coli R049 gene

ABSTRACT: The objective was to determine the function of the novel uropathogenic Escherichia coli (UPEC) gene R049 during host infection. We infected the urinary tracts of mice with E. coli UPEC132 or the R049 deletion mutant UPEC132ΔR049.The mouse kidneys were harvested at 4 and 8 h post-infection and screened for differentially expressed genes by microarray analysis. We identified 379 and 515 differentially expressed genes at 4 and 8 h post-infection, respectively. Thirty-four of these genes were associated with inflammatory and immune signaling pathways, including those related to mitogen-activated protein kinase signaling, leukocyte transendothelial migration, cytokine-cytokine receptor interaction, Toll-like receptor signaling, and apoptosis. Protein binding (GO 0005515) was the most prevalent molecular function in the Gene Ontology terms related to differentially expressed genes. In conclusion, R049 expression in UPEC132 is related to the early innate immune and inflammatory responses in UPEC-infected hosts. This work lays the foundation for further research on anti-infective immunity against UPEC.

ORGANISM(S): Mus musculus

PROVIDER: GSE63502 | GEO | 2014/11/21

SECONDARY ACCESSION(S): PRJNA268088

REPOSITORIES: GEO

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Functional analysis of the uropathogenic Escherichia coli R049 gene

Project description:The objective was to determine the function of the novel uropathogenic Escherichia coli (UPEC) gene R049 during host infection. We infected the urinary tracts of mice with E. coli UPEC132 or the R049 deletion mutant UPEC132ΔR049.The mouse kidneys were harvested at 4 and 8 h post-infection and screened for differentially expressed genes by microarray analysis. We identified 379 and 515 differentially expressed genes at 4 and 8 h post-infection, respectively. Thirty-four of these genes were associated with inflammatory and immune signaling pathways, including those related to mitogen-activated protein kinase signaling, leukocyte transendothelial migration, cytokine-cytokine receptor interaction, Toll-like receptor signaling, and apoptosis. Protein binding (GO 0005515) was the most prevalent molecular function in the Gene Ontology terms related to differentially expressed genes. In conclusion, R049 expression in UPEC132 is related to the early innate immune and inflammatory responses in UPEC-infected hosts. This work lays the foundation for further research on anti-infective immunity against UPEC. A ten chip study using total RNA recovered from 10 separate mouse kidneys of five experimental groups. The five experimental groups respectively were the UPEC132_4h group, UPEC132_8h group, UPEC132ΔR049_4h group, UPEC132ΔR049_8h group and Phosphate Buffered Saline (PBS) groups. Two separate mouse kidneys in every group were tested with two chips. Each chip measures the expression level of 44,170 genes from BALB/c mouse with three 60-mer probe pairs per gene.

2014-11-21 | E-GEOD-63502 | biostudies-arrayexpress

Expression data from human neutrophils exposed to uropathogenic and commensal Esherichia coli.

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2010-03-07 | E-GEOD-18810 | biostudies-arrayexpress

Expression data from human neutrophils exposed to uropathogenic and commensal Esherichia coli.

2010-03-01 | GSE18810 | GEO

Human renal fibroblasts are strong immunomobilizers during a urinary tract infection mediated by uropathogenic Escherichia coli

Project description:To prevent the onset of urosepsis and reduce mortality, a better understanding of how uropathogenic Escherichia coli (UPEC) manages to infiltrate the bloodstream through the kidneys is needed. The present study elucidates if human renal interstitial fibroblasts are part of the immune response limiting a UPEC infection, or if UPEC has the ability to modulate the fibroblasts for their own gain. Microarray results showed that upregulated genes were associated with an activated immune response. We also found that chemokines released from renal fibroblasts upon a UPEC infection could be mediated by LPS and triacylated lipoproteins activating the TLR2/1, TLR4, MAPK, NF-κB and PKC signaling pathways. Furthermore, UPEC was also shown to be able to adhere and invade renal fibroblasts, mediated by the P-fimbriae. Furthermore, it was found that renal fibroblasts were more immunoreactive than renal epithelial cells upon a UPEC infection. However, both renal fibroblasts and epithelial cells were equally efficient at inducing neutrophil migration. In conclusion, we have found that human renal fibroblasts can sense UPEC and mobilize a host response with neutrophil migration. This suggests that renal fibroblasts are not only structural cells that produce and regulate the extracellular matrix, but also highly immunoreactive cells.

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2022-06-09 | PXD032049 | Pride

DamX controls reversible cell morphology-switching in uropathogenic Escherichia coli.

Project description:Transcriptional analysis of UTI89 - uropathogenic E.coli (UPEC) strain grown in urine/Luria bertani medium culture in vitro as well as during three distinct phases of UPEC bladder infection: intracellular growth, filament formation and filament reversal. UTI89 was used to infect a bladder epithelial cell line cultured within a dynamic flow chamber system and harvested at particular stages of its pathogenecity cascade. Total RNA was processed and cy3 labeled for microarray analysis using Agilent custom Escherichia coli UTI89 arrays designed using E-Array.

2017-05-28 | E-MTAB-3611 | biostudies-arrayexpress

Uropathogenic Escherichia coli biofilm proteomics

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).

2021-04-01 | PXD023998 | Pride

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Project description:While in transit within and between hosts, uropathogenic E. coli (UPEC) encounter multiple stresses, including substantial levels of nitric oxide and reactive nitrogen intermediates. Strains of UPEC become conditioned to high concentrations of acidified sodium nitrite (ASN), a model system used to generate nitrosative stress. We used microarrays to define the expression profile of UPEC that have been conditioned for growth in ASN.

2009-03-21 | GSE15319 | GEO

Cell wall-deficient Mycoplasma hominis represses biofilm formation of uropathogenic Escherichia coli.

Project description:The features of Mycoplasma in human organ such lung and urinary tract are enigmatic. Here, the role of M. hominis in regard to biofilm formation of uropathogenic Escherichia coli (UPEC) strain CFT073 was investigated. Although M. hominis were inferred to not impact on UPEC bacterial fitness including growth and productions of signaling molecules as autoinducer-2 (AI-2) and indole, we found that the presence of M. hominis dramatically decreased biofilm formation of UPEC CFT073 as well as slightly repressed attachment and cytotoxicity of that. Importantly, this activity was observed on UPEC strain specifically, not enterohemorrhagic E. coli (EHEC) strain that exists on intestine. Whole-transcriptome profiling and quantitative real-time polymerase chain reaction (qRT-PCR) analysis revealed PhoPQ system and anti-termination protein (encoded by ybcQ) participates on the reduction of biofilm formation by M. hominis (corroborated by qRT-PCR). Furthermore, collaborating with previous report that toxin-antitoxin (TA) system involved in biofilm formation, M. hominis increased on the transcriptions of toxin genes including hha (toxin gene in Hha-TomB TA system) and pasT (toxin part in PasT-PasI TA system). Hence, we propose that one possible role of M. hominis is to influence bacterial biofilm formation in urinary tract. Only fourteen genes were induced (2.5-fold) by the presence of M. hominis in Uropathogenic Escherichia coli (UPEC) biofilm cells. Among upregulated genes, ybcQ (encodes anti-termination protein Q homolog) and phoP/phoQ (encode DNA-binding response regulators in two-component regulatory system), were induced by the presence of M. hominis. Two-condition experiment, UPEC CFT073 alone vs. UPEC CFT073 with Mycoplasma hominis PG21 (10^5 ccu/ml). For preparing the total RNA, UPEC CFT073 cells were grown at 37Â°C in biofilm cells on glass wool with or without M. hominis for 24 h.

2016-01-08 | E-GEOD-43376 | biostudies-arrayexpress

Genome-wide maping the chromatin status of 5637 cells following infection with Uropathogenic E.coli

Project description:We report the application of H3 Lysine9 acetylation (H3K9ac) immunoprecipitation coupled next generation sequencing (ChIP-seq) in human bladder epithelial cells 5637 following treatment with Urophathogenic Escherichia coli strain 536 (UPEC) or the mutant with deletion of both α-hemolysin (hlyA) genes in the UPEC 536 strain (hlyA double mutant = UPEC 536 HDM) or UPEC supplemented with acetate. We found dramatic depletion of H3K9ac peaks was observed in UPEC infected cells, which was partially rescued by supplementation of acetate. In contrast, H3K9ac peaks of untreated cells are comparable with HDM treated cells. A total 21834 merged peak regions were identified in untreated control, whilst UPEC infection significantly decreased the signal across the merged peak regions, which was rescued partially by adding acetate. Deacetylation and its rescue by addition of acetate were observed in a global manner and affected the vast majority of H3K9ac sites throughout the genome. This observation holds true for different classes of cis-regulatory elements. Analysis of average binding across all human transcriptional start sites analysis further revealed that UPEC treatment also decrease H3K9ac signals at promoter regions, and can be rescue by supplementation of acetate. Moreover H3K9ac signal is also correlated with gene expression pattern. This study established that UPEC infection could epigenetically manipulate the host cell gene expression.

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