Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Xenophagic process controls the Enteroinvasive Escherichia coli infection of the epithelial cells II

ABSTRACT: The invasive bacteria recognition by host cells through autophagy is a key factor for determining bacterial infection. Enteroinvasive Escherichia coli (EIEC) express a protein IcsB, which in Shigella, is known for inactivating the bacterial degradation process. Once EIEC showed less expression of icsB when compared to S. flexneri, we proposed to investigate the autophagy caused by EIEC infection. Our results showed that IcsB protein is an important virulence factor in EIEC because it causes a camouflage of the bacteria in the eukaryotic cell. When there is low or none expression of the protein, the cell recognition of the invasive bacteria is high, decreasing the bacteria dissemination. This found confirms the importance of the gene transcription and the sequence, since the strain E. coli SM124/13, complemented with icsB from Shigella, showed higher dissemination efficiency inside of the host cell. Additionally, our results revealed that eukaryotic cell infected by EIEC or Shigella flexneri showed distinguish responses. In EIEC infection, the autophagy was activated in human cells, but not in a conventional mode. Our hypothesis is that EIEC is recognized by autophagy, being an important cell process for bacterial recognition.

ORGANISM(S): Homo sapiens

PROVIDER: GSE93587 | GEO | 2020/01/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Xenophagic process controls the Enteroinvasive Escherichia coli infection of the epithelial cells I

Project description:The invasive bacteria recognition by host cells through autophagy is a key factor for determining bacterial infection. Enteroinvasive Escherichia coli (EIEC) express a protein IcsB, which in Shigella, is known for inactivating the bacterial degradation process. Once EIEC showed less expression of icsB when compared to S. flexneri, we proposed to investigate the autophagy caused by EIEC infection. Our results showed that IcsB protein is an important virulence factor in EIEC because it causes a camouflage of the bacteria in the eukaryotic cell. When there is low or none expression of the protein, the cell recognition of the invasive bacteria is high, decreasing the bacteria dissemination. This found confirms the importance of the gene transcription and the sequence, since the strain E. coli SM124/13, complemented with icsB from Shigella, showed higher dissemination efficiency inside of the host cell. Additionally, our results revealed that eukaryotic cell infected by EIEC or Shigella flexneri showed distinguish responses. In EIEC infection, the autophagy was activated in human cells, but not in a conventional mode. Our hypothesis is that EIEC is recognized by autophagy, being an important cell process for bacterial recognition.

2020-01-11 | GSE93525 | GEO

Xenophagic process controls the Enteroinvasive Escherichia coli infection of the epithelial cells III

2020-01-11 | GSE93588 | GEO

Dual-transcriptome of Shigella flexneri infecting human HCT116 cells

Project description:Analyse the transcriptionnal changes of human colon epithelial cells (HCT116) associated with Shigella flexneri (M90T) infection and correlated with the bacterial transcriptional program.

2024-12-01 | E-MTAB-14119 | biostudies-arrayexpress

The expression profiles analysis of a virulence plasmid-cured strain of shigella flexneri

2008-12-22 | GSE12535 | GEO

Transcriptomic profiling of HeLa cells infected with Shigella flexneri

Project description:We evaluated the transcriptome changes induced by infection of Hela 229 cells with Shigella flexneri. The sample set consists of a control (mock), total population of infected sample and infected sample sorted into Shigella positive and Shigella negative population.

2017-04-04 | GSE75746 | GEO

Detection of Q-modification in RNAs from S. pombe and S. flexneri via reverse transcription using RT-KTq I614Y (Q-MaP-Seq)

Project description:In most eukaryotes and bacteria, queuosine (Q) replaces the guanosine at the wobble position of tRNAs harboring a GUN anticodon. To faithfully detect Q-modification in RNAs from Schizosaccharomyces pombe and Shigella flexneri, Q-MaP-Seq was established and applied to tRNAs from S. pombe WT (AEP1) cells and Shigella flexneri WT cells and tgt∆ cells. Q-modification of in vitro-transcribed RNAs and RNAs isolated from S. pombe and S. flexneri followed by reverse transcription using the RT-active DNA polymerase variant RT-KTq I614Y and sequencing of unmodified compared to modified RNAs allowed identification of Q-sites within tRNAs.

2023-03-15 | GSE216921 | GEO

miRNA profiling of human colon cells infected with the bacterium Shigella flexneri

Project description:Overview of microRNA expression changes during Shigella flexneri infection of human colon epithelial cells (HCT116)

2024-12-01 | E-MTAB-14092 | biostudies-arrayexpress

LC-MS/MS of the secreted fraction of Shigella

Project description:Many human Gram-negative bacterial pathogens express a Type Three Secretion Apparatus (T3SA), including among the most notorious Shigella spp., Salmonella enterica, Yersinia enterocolitica and enteropathogenic Escherichia coli (EPEC). These bacteria express on their surface multiple copies of the T3SA that mediate the delivery into host cells of specific protein substrates critical to pathogenesis. Shigella spp. are Gram-negative bacterial pathogens responsible for human bacillary dysentery. The effector function of several Shigella T3SA substrates has largely been studied but their potential cellular targets are far from having been comprehensively delineated. In addition, it is likely that some T3SA substrates have escaped scrutiny as yet. Indeed, sequencing of the virulence plasmid of Shigella flexneri has revealed numerous open reading frames with unknown functions that could encode additional T3SA substrates. Taking advantage of label-free mass spectrometry detection of proteins secreted by a constitutively secreting strain of S. flexneri, we identified five novel substrates of the T3SA. We further confirmed their secretion through the T3SA and translocation into host cells using b-lactamase assays. The coding sequences of two of these novel T3SA substrates (Orf13 and Orf131a) have a guanine-cytosine content comparable to those of T3SA components and effectors. The three other T3SA substrates identified (Orf48, Orf86 and Orf176) have significant homology with antitoxin moieties of type II Toxin-Antitoxin systems usually implicated in the maintenance of low copy plasmids. While Orf13 and Orf131a might constitute new virulence effectors contributing to S. flexneri pathogenicity, potential roles for the translocation into host cells of antitoxins or antitoxin-like proteins during Shigella infection are discussed.

2017-10-17 | PXD006086 | Pride

Dual RNA-seq of zebrafish larvae infected with Shigella sonnei

Project description:Shigella flexneri is historically regarded as the primary agent of bacillary dysentery, yet the closely-related Shigella sonnei is replacing S. flexneri, especially in developing countries. The underlying reasons for this dramatic shift are mostly unknown. Using a zebrafish (Danio rerio) model of Shigella infection, we discover that S. sonnei is more virulent than S. flexneri in vivo. Whole animal dual-RNAseq and testing of bacterial mutants suggest that S. sonnei virulence depends on its O-antigen oligosaccharide (which is unique among Shigella species). We show in vivo using zebrafish and ex vivo using human neutrophils that S. sonnei O-antigen can mediate neutrophil tolerance. Consistent with this, we demonstrate that O-antigen enables S. sonnei to resist phagolysosome acidification and promotes neutrophil cell death. Chemical inhibition or promotion of phagolysosome maturation respectively decreases and increases neutrophil control of S. sonnei and zebrafish survival. Strikingly, larvae primed with a sublethal dose of S. sonnei are protected against a secondary lethal dose of S. sonnei in an O-antigen-dependent manner, indicating that exposure to O-antigen can train the innate immune system against S. sonnei. Collectively, these findings reveal O-antigen as an important therapeutic target against bacillary dysentery, and may explain the rapidly increasing S. sonnei burden in developing countries.

2019-11-19 | GSE140544 | GEO

The expression profiles analysis of a virulence plasmid-cured strain of shigella flexneri

Project description:In this study, we analyzed the expression profiles of a virulence plasmid-cured strain and wild-type strain of shigella flexneri. The results showed that the genes of glp regulon were upregulated in mutant bacteria in stationary phase cultures. The two strains were cultured in LB broth into log-phase and stationary phase respectively. Then, the total RNAs were extracted and analyzed by Nimblegen biochips.

2010-05-15 | E-GEOD-12535 | biostudies-arrayexpress

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