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PROVIDER: PRJNA973688 | ENA |
REPOSITORIES: ENA
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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
Project description:Typical enteropathogenic Escherichia coli (EPEC) O55:H7 is regarded as the closest relative of enterohemorrhagic E. coli (EHEC) O157:H7. Both serotypes usually express the γ1 intimin subclass and trigger actin polymerazation by the Tir-TccP pathway. However, atypical O55:H7 strains capable of triggering actin polymerization via the Tir-Nck pathway have recently been identified. In this study, we investigated the genotypic differences and phylogenetic relationships between typical and atypical O55:H7 strains. We show that the atypical O55:H7 strains, which express the θ intimin subclass and lack both tccP and tccP2, belong to an E. coli lineage distinct from the typical O55:H7 and from the EPEC O55:H6, which also uses the Tir-Nck actin polymerization pathway. We conducted genomic comparisons of the chromosomal regions covering the O-antigen gene cluster and its flanking regions between the three O55 lineages by restriction fragment length polymorphism analysis of PCR products and DNA sequencing analysis of about 65-kb chromosomal regions. This unexpectedly revealed that horizontal transfer of large fragments (≥ 40 kb) encoding the O55-antigen gene cluster and part of neighboring colanic acid gene cluster is involved in the emergence of the three O55 E. coli lineages. The data provide new insights into the mechanisms involved in the generation of a wide variety of O-serotypes in Gram-negative bacteria. Keywords: comparative genomic hybridization
2008-04-01 | GSE8889 | GEO
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
Project description:Typical enteropathogenic Escherichia coli (EPEC) O55:H7 is regarded as the closest relative of enterohemorrhagic E. coli (EHEC) O157:H7. Both serotypes usually express the γ1 intimin subclass and trigger actin polymerazation by the Tir-TccP pathway. However, atypical O55:H7 strains capable of triggering actin polymerization via the Tir-Nck pathway have recently been identified. In this study, we investigated the genotypic differences and phylogenetic relationships between typical and atypical O55:H7 strains. We show that the atypical O55:H7 strains, which express the θ intimin subclass and lack both tccP and tccP2, belong to an E. coli lineage distinct from the typical O55:H7 and from the EPEC O55:H6, which also uses the Tir-Nck actin polymerization pathway. We conducted genomic comparisons of the chromosomal regions covering the O-antigen gene cluster and its flanking regions between the three O55 lineages by restriction fragment length polymorphism analysis of PCR products and DNA sequencing analysis of about 65-kb chromosomal regions. This unexpectedly revealed that horizontal transfer of large fragments (⥠40 kb) encoding the O55-antigen gene cluster and part of neighboring colanic acid gene cluster is involved in the emergence of the three O55 E. coli lineages. The data provide new insights into the mechanisms involved in the generation of a wide variety of O-serotypes in Gram-negative bacteria. Keywords: comparative genomic hybridization Total 8 test samples were analyzed. Genomic DNA from each test strain and a reference strain (O157 Sakai) were labeled with Cy3 and Cy5, respectively, and were cohybridized on a single array. Labeling and hybridization were performed twice independently.
2010-05-22 | E-GEOD-8889 | biostudies-arrayexpress
Project description:To define the impact of asymptomatic malaria, we pursued a systems approach integrating antibody responses, mass cytometry, and transcriptional profiling of individuals experiencing symptomatic and asymptomatic P. falciparum infection. Defined populations of classical and atypical memory B cells and a TH2 cell bias were associated with reduced risk of clinical malaria. Despite these protective responses, asymptomatic malaria featured an immunosuppressive transcriptional signature with upregulation of pathways involved in the inhibition of T cell function, and CTLA-4 as a predicted regulator in these processes.
2022-02-21 | GSE181179 | GEO
Project description:Global transcriptional analysis of eleven EPEC strains, including the most frequently studied strains used in laboratory studies investigating EPEC virulence mechanisms.
2017-05-10 | GSE73885 | GEO
Project description:We employed a genome-wide microarray approach to obtain a profile of the transcriptional events in ciprofloxacin-treated EPEC shedding light on how ciprofloxacin affects EPEC transcriptional events and growth, aside from resistance mechanisms, and how this bacterium tolerates antibiotic stress. Sample of each culture immediately after the addition of ciprofloxacin (t0), 45 min (t45), 90 min (t90), 135 min (t135), and 180 min (t180), ciprofloxacin induced gene expression in EPEC Deng strain were measure by microarray statistical analysis
2015-12-15 | E-GEOD-75988 | biostudies-arrayexpress