Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Adaptation of commensal proliferating Escherichia coli to the intestinal tract of young children with cystic fibrosis

ABSTRACT: Adaptation of commensal proliferating Escherichia coli to the intestinal tract of young children with cystic fibrosis

PROVIDER: PRJNA428927 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6449110.fastq.gz	Fastqsanger.gz
	SRR6449120.fastq.gz	Fastqsanger.gz
	SRR6449111.fastq.gz	Fastqsanger.gz
	SRR6449121.fastq.gz	Fastqsanger.gz
	SRR6449112.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Adaptation of commensal proliferating Escherichia coli to the intestinal tract of young children with cystic fibrosis

Project description:E. coli isolates from different CF patients demonstrate increased growth rate when grown with glycerol, a major component of fecal fat, as the sole carbon source compared to E. coli from healthy controls. CF and control E. coli isolates have differential gene expression when grown in minimal media with glycerol as the sole carbon source. While CF isolates display a growth promoting transcriptional profile, control isolates engage stress and stationary phase programs, which likely results in slower growth rates.

2018-01-09 | GSE108846 | GEO

Adaptation of commensal proliferating <i>Escherichia coli</i> to the intestinal tract of young children with cystic fibrosis.

Project description:The mature human gut microbiota is established during the first years of life, and altered intestinal microbiomes have been associated with several human health disorders. Escherichia coli usually represents less than 1% of the human intestinal microbiome, whereas in cystic fibrosis (CF), greater than 50% relative abundance is common and correlates with intestinal inflammation and fecal fat malabsorption. Despite the proliferation of E. coli and other Proteobacteria in conditions involving chronic gastrointestinal tract inflammation, little is known about adaptation of specific characteristics associated with microbiota clonal expansion. We show that E. coli isolated from fecal samples of young children with CF has adapted to growth on glycerol, a major component of fecal fat. E. coli isolates from different CF patients demonstrate an increased growth rate in the presence of glycerol compared with E. coli from healthy controls, and unrelated CF E. coli strains have independently acquired this growth trait. Furthermore, CF and control E. coli isolates have differential gene expression when grown in minimal media with glycerol as the sole carbon source. While CF isolates display a growth-promoting transcriptional profile, control isolates engage stress and stationary-phase programs, which likely results in slower growth rates. Our results indicate that there is selection of unique characteristics within the microbiome of individuals with CF, which could contribute to individual disease outcomes.

| S-EPMC5816161 | biostudies-literature

Environmental exposures and inflammation in young children with cystic fibrosis

Project description:Secondhand smoke exposure (SHSe) is a common environmental factor known to increase asthma severity and respiratory infections in children, as well disrupt metabolic signals and host immune responses in patients with cystic fibrosis (CF). This study defines biomarkers and metabolic profiles of SHSe (includes ENDS exposure) in the young CF population and determines how SHSe impacts regulation of infection, inflammation, and respiratory health.

2018-10-10 | ST001079 | MetabolomicsWorkbench

Gene expression profile at single cell level of a rare seen and young tracheal adenoid cystic carcinoma

Project description:tracheal adenoid cystic carcinoma is one kind of non-small-cell lung cancer with limit treatment options. We used single cell RNA sequencing (scRNA-seq) to analyze the molecular characteristic of tracheal adenoid cystic carcinoma, aiming to recognized this disease deeply and provide potential treatment plan in the future.

2024-10-31 | GSE245170 | GEO

Transcriptional adaptation to cystic fibrosis transmembrane conductance regulator deficiency

Project description:Cystic fibrosis, the most commonly inherited lethal pulmonary disorder in Caucasians, is caused by mutations in the cystic fibrosis transmembrane conductance regulator gene (CFTR). To identify genomic responses to the presence or absence of CFTR in pulmonary tissues in vivo, microarray analyses of lung mRNAs were performed on whole lung tissue from mice lacking (CFTR(-)) or expressing mouse CFTR (CFTR(+)). Whereas the histology of lungs from CFTR(-) and CFTR(+) mice was indistinguishable, statistically significant increases in the relative abundance of 29 and decreases in 25 RNAs were identified by RNA microarray analysis. Of RNAs whose expression was consistently altered by the absence of CFTR, functional classes of genes influencing gene transcription, inflammation, intracellular trafficking, signal transduction, and ion transport were identified. RNAs encoding the transcription factor CCAAT enhancer-binding protein (CEBP) delta and interleukin (IL) 1beta, both known to regulate CFTR expression, were induced, perhaps indicating adaptation to the lack of CFTR. RNAs mediating lung inflammation including calgranulin-S100 family members, IL-1beta and IL-4, were increased. Likewise, expression of several membrane transport proteins that interact directly with CFTR were increased, suggesting that CFTR-protein complexes initiate genomic responses. Absence of CFTR influenced the expression of genes modulating diverse pulmonary cell functions that may ameliorate or contribute to the pathogenesis of CF. Keywords: Genotype comparison

2006-03-24 | GSE4513 | GEO

Commensal MGE Transfer

Project description:Commensal MGE Transfer

| PRJEB49256 | ENA

The lung microbiome in young children with cystic fibrosis: a longitudinal cohort study

Project description:The lung microbiome in young children with cystic fibrosis: a longitudinal cohort study

| PRJEB28588 | ENA

Pseudomonas aeruginosa lasR mutants in young cystic fibrosis patients

Project description:Pseudomonas aeruginosa undergoes genetic change during chronic infection of the airways of cystic fibrosis (CF) patients. One common change is mutation of lasR. LasR is a transcriptional regulator that responds to one of the quorum sensing signals in P. aeruginosa, and regulates acute virulence factor expression as well as central metabolic functions. P. aeruginosa mutants in which lasR was inactivated emerged in the airways of CF patients early during chronic infection, and during growth in the laboratory on Luria-Bertani agar. Both environments are rich in amino acids. Inactivation of lasR in these isolates conferred a growth advantage with amino acids, a phenotype that could account for selection of lasR mutants both in vivo and in vitro. P. aeruginosa lasR mutants were identified by their distinctive colony morphology, including autolysis that correlated with an imbalance in 4-hydroxy-2-alkylquinolines (HAQs), and an iridescent metallic sheen likely caused by the accumulation of one such HAQ. The alterations in transcriptional profile due to inactivation of lasR were conserved in isolates from multiple young CF patients. P. aeruginosa lasR mutations may represent surrogate markers to delineate stages in the natural history of CF airway disease, each with different prognostic and therapeutic implications, analogous to the markers used to direct cancer treatment. Similar to cancer cell mutations that promote unrestricted growth, lasR mutations may promote unrestricted growth of P. aeruginosa in the CF airway by enabling more efficient utilization of available amino acids. Analyse the effects of mutation of the lasR gene in Pseudomonas aeruginosa isolates from cystic fibrosis patients by comparing the transcriptional profile of an isolate from a young patient with that of an isogenic engineered lasR mutant.

2010-06-30 | E-GEOD-5560 | biostudies-arrayexpress

Effects of pathogen-commensal co-infection in cystic fibrosis

Project description:In this study, we performed infection studies of murine precision cut lung slices (PCLS) with P. aeruginosa and commensal bacteria isolated from cystic fibrosis airway samples to study the effects of co-infection.

| PRJEB48894 | ENA

Interactions with Commensal or Non-commensal Streptococci Alter Streptococcus mutans Transcriptome and Behaviors

Project description:RNA-Seq was used to compare the transcriptome of Streptococcus mutans UA159 during growth alone in monoculture, in coculture with Streptococcus gordonii DL1, Streptococcus sanguinis SK36 or Streptococcus oralis 34, and in a quadculture containing all four species. Individual cultures of commensal species Streptococcus gordonii DL1, Streptococcus sanguinis SK36 and Streptococcus oralis 34 were sequenced as well. This revealed a common transcriptome pattern in S. mutans when grown in mixed-species culture, indepenedent of the species identity that S. mutans was cultured with. Additionally, transcriptome changes in the commensal species could also be determined when undergoing competition from S. mutans. RNA-Seq was used to compare the transcriptome of Streptococcus mutans UA159 during growth alone in monoculture or in coculture with Streptococcus sobrinus NIDR 6715, Lactobacillus casei ATCC 4646 or Corynebacterium matruchotii ATCC 14266. These data were compared to previous coculture and quadculture RNA-Seq data with commensal streptococci (GSE209925). These data confirmed a common transcriptome pattern in S. mutans when grown in mixed-species culture with commensal streptococci that is not present with non-commensal streptococci, indepenedent of the species identity that S. mutans was cultured with.

2022-08-03 | GSE209925 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data