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Transcriptomic profiles of host epithelial cells in response to actin rearrangement induced by atypical enteropathogenic Escherichia coli

ABSTRACT: Transcriptomic profiles of host epithelial cells in response to actin rearrangement induced by atypical enteropathogenic Escherichia coli

PROVIDER: PRJNA593509 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10587352.fastq.gz	Fastqsanger.gz
	SRR10587353.fastq.gz	Fastqsanger.gz
	SRR10587354.fastq.gz	Fastqsanger.gz
	SRR10587355.fastq.gz	Fastqsanger.gz
	SRR10587356.fastq.gz	Fastqsanger.gz

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Transcriptomic profiles of host epithelial cells in response to actin rearrangement induced by atypical enteropathogenic Escherichia coli

Project description:Atypical enteropathogenic Escherichia coli (aEPEC) is amongst the leading causes of diarrheal disease worldwide. The colonization of the gut mucosa by aEPEC results in actin pedestal formation at the site of bacterial attachment. This cytoskeletal rearrangement is triggered by the interaction between the bacterial adhesin intimin and its receptor Tir, which is translocated through the type three secretion system, to the host cell. While some aEPEC require tyrosine phosphorylation of Tir and recruitment of the host Nck to trigger actin polymerization, certain aEPEC strains, whose Tir is not phosphorylated, rely on the effector EspFu for efficient actin remodeling. To understand how the host responds to these different actin polymerization signaling pathways, we analyzed gene expression changes in epithelial cells infected with pedestal-forming aEPEC strains using high-throughput RNA sequencing (RNA-seq).

2020-04-01 | GSE141446 | GEO

Atypical enteropathogenic E. coli virulence markers

Project description:Atypical enteropathogenic E. coli virulence markers

| PRJEB2827 | ENA

Atypical Enteropathogenic Escherichia coli Virulence Regulation by QseC Quorum Sensing Adrenergic Sensor

Project description:Atypical EPEC (aEPEC) strains are part of group of pathogens capable of forming the Attaching and Effacing (A/E) lesion. This lesion is characterized by intimate adherence of bacteria to enterocytes, and microvilli destruction. The genes responsible to cause that lesion are located in a pathogenicity island called Locus of Enterocyte Effacement (LEE). Transcription of LEE genes is subjected to various levels of regulation, including quorum sensing through autoinducer 3 (AI-3) system. AI-3 is an aromatic compound with similar characteristics to the epinephrine and norepinephrine hormones. This similarity allows bacteria to use these hormones and AI-3 to perform cell M-bM-^@M-^S to M-bM-^@M-^S cell signaling processes and bacteria - host communication processes in order to modulate its virulence. AI-3, epinephrine and norepinephrine are detected by a sensor kinase named quorum sensing E.coli regulator (QseC). In order to investigate the role of QseC and epinephrine in atypical EPEC O55:H7 virulence, we constructed a QseC mutant of this strain and performed transcription and phenotypic analyses in the presence or absence of epinephrine. We have reported here, for the first time, the quorum sensing QseC regulation of virulence genes in atypical EPEC. Our results shown that QseC is a global regulator of gene expression in aEPEC and positively regulates flagellar genes, LEE and non-LEE encoded factors. We also have shown that the presence of epinephrine could be sensed by other receptor that acts as negative regulator of LEE4 and LEE5 genes. Comparison of transcriptional regulation of enteropathogenic E. coli serotype O55:H7 wild type and the qseC mutant in the absence or presence of epinephrine signal to identify the regulated targets

2013-01-08 | E-GEOD-43325 | biostudies-arrayexpress

Atypical Enteropathogenic Escherichia coli Virulence Regulation by QseC Quorum Sensing Adrenergic Sensor

Project description:Atypical EPEC (aEPEC) strains are part of group of pathogens capable of forming the Attaching and Effacing (A/E) lesion. This lesion is characterized by intimate adherence of bacteria to enterocytes, and microvilli destruction. The genes responsible to cause that lesion are located in a pathogenicity island called Locus of Enterocyte Effacement (LEE). Transcription of LEE genes is subjected to various levels of regulation, including quorum sensing through autoinducer 3 (AI-3) system. AI-3 is an aromatic compound with similar characteristics to the epinephrine and norepinephrine hormones. This similarity allows bacteria to use these hormones and AI-3 to perform cell – to – cell signaling processes and bacteria - host communication processes in order to modulate its virulence. AI-3, epinephrine and norepinephrine are detected by a sensor kinase named quorum sensing E.coli regulator (QseC). In order to investigate the role of QseC and epinephrine in atypical EPEC O55:H7 virulence, we constructed a QseC mutant of this strain and performed transcription and phenotypic analyses in the presence or absence of epinephrine. We have reported here, for the first time, the quorum sensing QseC regulation of virulence genes in atypical EPEC. Our results shown that QseC is a global regulator of gene expression in aEPEC and positively regulates flagellar genes, LEE and non-LEE encoded factors. We also have shown that the presence of epinephrine could be sensed by other receptor that acts as negative regulator of LEE4 and LEE5 genes.

2013-01-08 | GSE43325 | GEO

Comparative genome hybridization of Enteropathogenic Yersinia

Project description:Enteropathogenic Yersinia enterocolitica and Yersinia pseudotuberculosis share many traits in terms of infections they cause, but their epidemiology and ecology seem to differ in many ways. Pigs are the only known reservoir for Y. enterocolitica 4/O:3 strains while Y. pseudotuberculosis strains have been isolated from variety of sources including fresh vegetables and wild animals. A comparative genomic hybridization (CGH) analysis with a DNA microarray based on three Yersinia enterocolitica and four Yersinia pseudotuberculosis genomes was conducted to shed light on genomic differences between the enteropathogenic Yersinia. In total 99 strains isolated from various sources were hybridized and analyzed.

2015-10-01 | GSE67565 | GEO

Escherichia coli E110019

Project description:Atypical enteropathogenic Escherichia coli

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The RegR virulence regulon of rabbit specific enteropathogenic Escherichia coli strain E22

Project description:To investigate the regulatory targets of the RegR virulence regulon of rabbit specific enteropathogenic Escherichia coli strain E22

2012-12-25 | GSE41093 | GEO

The RegR virulence regulon of rabbit specific enteropathogenic Escherichia coli strain E22

Project description:To investigate the regulatory targets of the RegR virulence regulon of rabbit specific enteropathogenic Escherichia coli strain E22 Single factor (genotype) with dye swaps.

2012-12-25 | E-GEOD-41093 | biostudies-arrayexpress

Comparative genome hybridization of Enteropathogenic Yersinia

Project description:Comparative genome hybridization of Enteropathogenic Yersinia

| PRJNA280273 | ENA

Variation in the Genomic islands of porcine enteropathogenic E. coli strains of serogroup O45 revealed by CGH and PCR.

Project description:Background: Members of E. coli serogroup O45 are porcine enteropathogenic E. coli (PEPEC) strains which cause post-weaning diarrhea and produce characteristic attaching and effacing (A/E) lesions. Most of O45 PEPEC strains possess the locus of enterocyte effacement (LEE), encoding the virulence factors for A/E lesions, and often possess the paa gene, which is thought to contribute to the early stages of PEPEC virulence. Methodology: Nine O45 PEPEC strains and a rabbit enteropathogenic (REPEC) strain, known to produce A/E lesions, were characterized using an E. coli O157-E. coli K12 whole genome microarray and a virulence gene-specific microarray, and by PCR experiments. Results: Based on their virulence genes profiles, the 10 strains were characterized as atypical EPEC. The differences in their genomes pointed to two distinct evolutionary groups of O45 PEPEC, Group I and Group II, and to the contribution these genetic differences have on virulence in pigs. Group I contained the REPEC strain and four O45 PEPEC strains known to induce severe A/E lesions in challenged pigs whereas Group II was composed of five other O45 PEPEC strains which induced less severe or no A/E lesions in challenged pigs. Significant differences between Groups I and II were found in the presence or absence of 50 O-Islands (OIs) or S-loops and 13 K-islands (KIs) or K-loops, including the virulence-associated islands OI#1 (S-loop#1), OI#47 (S-loop#71), OI#57 (S-loop#85), OI#71 (S-loop#108), OI#115, OI#122, and OI#154 (S-loop#253). 10 samples, with two microarrays per sample. Each microarray includes duplicates of every spot.

2010-05-16 | E-GEOD-17036 | biostudies-arrayexpress

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