Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA291820 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Clustering of the Enteropathogenic (EPEC) Escherichia coli Tir effector, induced by its binding to Intimin, leads to pyroptotic cell death in macrophages. The effect of Tir clustering following EPEC infection of epithelial cells remains unexplored. In this study, we show that EPEC induces pyroptosis in an intestinal epithelial cell (IEC) line, in a Tir-dependent but actin polymerisation-independent manner, which was enhanced by priming with IFNγ. Mechanistically, Tir clustering induces rapid Ca2+ influx, which promotes internalisation of LPS, followed by activation of caspase-4. Chelation of extracellular Ca2+ or knockdown of caspase-4 inhibited cell death upon EPEC infection, whereas ATP-induced extracellular Ca2+ influx had the opposite effect confirming the regulatory role of calcium in the pathway. Additionally, IEC lines with low endogenous expression of caspase-4 were resistant to EPEC-induced cell death. We reveal a novel mechanism of LPS internalisation, following infection with an extracellular pathogen, leading to pyroptosis in IECs.
2020-10-28 | PXD018763 | Pride
Project description:Enterohemorrhagic Escherichia coli (EHEC) is a gram negative enteric bacterial pathogen that can cause hemorrhagic colitis and heamolytic uremic syndrome (HUS) in humans and is the cause of bloody diarrhoea and acute renal failure in children. We have studied the transcriptional response of a colon cell line (CaCo2) to infection by EHEC and another closely related enteric pathogen Enteropathogenic Escherichia coli (EPEC) and compared its response to a cervical cell line (Hela). We carried out microarray analysis on CaCo2 infected with EHEC O157H:7 EDL933 and EPEC E2348/69 at 4 hours of infection and analysis on Hela infected with EHEC also at 4 hours of infection
2016-09-01 | GSE13403 | GEO
Project description:Despite the characterization of many aetiologic genetic changes. The specific causative factors in the development of sporadic colorectal cancer remain unclear. This study was performed to detect the possible role of Enteropathogenic Escherichia coli (EPEC) in developing colorectal carcinoma.
| 2184564 | ecrin-mdr-crc
Project description:Enterohemorrhagic Escherichia coli (EHEC) is a gram negative enteric bacterial pathogen that can cause hemorrhagic colitis and heamolytic uremic syndrome (HUS) in humans and is the cause of bloody diarrhoea and acute renal failure in children. We have studied the transcriptional response of a colon cell line (CaCo2) to infection by EHEC and another closely related enteric pathogen Enteropathogenic Escherichia coli (EPEC) and compared its response to a cervical cell line (Hela). We carried out microarray analysis on CaCo2 infected with EHEC O157H:7 EDL933 and EPEC E2348/69 at 4 hours of infection and analysis on Hela infected with EHEC also at 4 hours of infection CaCo2 cells and Hela cells were grown to 80% confluency and infected with the bacteria for 4 hours before samples were collected for microarray analysis.
2016-09-01 | E-GEOD-13403 | biostudies-arrayexpress
Project description:Opioids analgesics are frequently prescribed in the United States and worldwide. However, serious side effects such as addiction, immunosuppression and gastrointestinal symptoms limit their use. It has been recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. Further study indicated distinct alterations in the gut microbiome and metabolome following morphine treatment, contributing to the negative consequences associated with opioid use. However, it is unclear how opioids modulate gut homeostasis in the context of a hospital acquired bacterial infection. In the current study, a mouse model of C. rodentium infection was used to investigate the role of morphine in the modulation of gut homeostasis in the context of a hospital acquired bacterial infection. Citrobacter rodentium is a natural mouse pathogen that models intestinal infection by enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) and causes attaching and effacing lesions and colonic hyperplasia. Morphine treatment resulted in 1) the promotion of C. rodentium systemic dissemination, 2) increase in virulence factors expression with C. rodentium colonization in intestinal contents, 3) altered gut microbiome, 4) damaged integrity of gut epithelial barrier function, 5) inhibition of C. rodentium-induced increase in goblet cells, and 6) dysregulated IL-17A immune response. This is the first study to demonstrate that morphine promotes pathogen dissemination in the context of intestinal C. rodentium infection, indicating morphine modulates virulence factor-mediated adhesion of pathogenic bacteria and induces disruption of mucosal host defense during C. rodentium intestinal infection in mice. This study demonstrates and further validates a positive correlation between opioid drug use/abuse and increased risk of infections, suggesting over-prescription of opioids may increase the risk in the emergence of pathogenic strains and should be used cautiously. Therapeutics directed at maintaining gut homeostasis during opioid use may reduce the comorbidities associated with opioid use for pain management.
2020-02-18 | E-MTAB-7503 | biostudies-arrayexpress
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
Project description:Enterohemorrhagic Escherichia coli (EHEC) induces the attachment and effacement of intestinal microvilli. While the molecular mechanisms contributed to the attachment of EHEC have been thoroughly studied, the underlying mechanisms for the effacement of intestinal microvilli induced by EHEC remained elusive. By focus RNAi screening and genetic analysis in C. elegans and further reconfirmed in human Caco-2 intestinal epithelial cells, we demonstrate that the CDK1-formin signal axis is required for this EHEC-induced microvillar effacement in vitro and in vivo.
2020-11-11 | GSE142507 | GEO
Project description:The inhibition of host innate immunity pathways is essential for the survival of attaching and effacing (A/E) pathogens such as enteropathogenic Escherichia coli (EPEC) and Citrobacter rodentium during mammalian infections. To subvert these pathways, A/E pathogens utilize a type III secretion system (T3SS) to introduce effectors that target key signaling pathways thereby suppressing the anti-microbial response. One effector used by A/E pathogens is the arginine glycosyltransferase NleB1 (NleBCR in C. rodentium) that modifies conserved arginine residues with N-acetylglucosamine (GlcNAc) in death-domain containing host proteins thereby blocking extrinsic apoptosis signaling. When expressed ectopically, NleB1 modifies the host proteins, FADD, TRADD and RIPK1. However, the true repertoire of arginine-GlcNAcylation during infection with endogenous levels of NleB delivered by the pathogen is unknown. Here we explored the effects of arginine-GlcNAcylation by NleB on the global host proteome. Utilizing an affinity proteomic approach for Arginine-GlcNAcylated glycopeptide, we compared the global repertoire of arginine-GlcNAcylation during ectopic expression of NleB, EPEC infection in vitro or C. rodentium infection in vivo. When NleB was overexpressed, multiple host proteins were arginine-GlcNAcylated. However, when endogenous levels of NleB were delivered during EPEC and C. rodentium infection, R117of FADD was rapidly and preferentially modified. The arginine-GlcNAcylation modification of FADD was extremely stable and insensitive to environmental or host cell degradation. Despite its stability and effect on the inhibition of apoptosis, arginine-GlcNAcylation did not illicit any proteomic changes, even in response to prolonged expression of NleB. Thus, under wild type levels of expression, NleB1/NleBCR antagonizes death-receptor-induced apoptosis of infected cells by modifying FADD in an irreversible and silent manner.
2017-09-11 | PXD006810 | Pride
Project description:Transcriptional Response to Ciprofloxacin in Enteropathogenic Escherichia coli Deng
| PRJNA305914 | ENA
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