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Cell type dependent comparison and strain specific comparison

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Nil Turan

PROVIDER: E-GEOD-13403 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Cell type dependent comparison and strain specific comparison

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

Comparison of acid treated and untreated

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 compared its profile to infection by EHEC shocked in acid at pH 2.5. We carried out microarray analysis on CaCo2 infected with EHEC O157H:7 EDL933 and EHEC shocked at pH 2.5 at 4 hours post infection.

2016-09-01 | GSE13404 | GEO

Comparison of acid treated and untreated

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 compared its profile to infection by EHEC shocked in acid at pH 2.5. We carried out microarray analysis on CaCo2 infected with EHEC O157H:7 EDL933 and EHEC shocked at pH 2.5 at 4 hours post infection. CaCo2 cells were grown to 80% confluency and infected with acid shocked and unschocked bacteria for 4 hours before samples were collected for microarray analysis.

2016-09-01 | E-GEOD-13404 | biostudies-arrayexpress

The type III secretion system effector EspO of enterohemorrhagic Escherichia coli inhibits apoptosis through an interaction with HAX-1

Project description:Many enteric pathogens employ a type III secretion system (T3SS) to translocate effector proteins directly into the host cell cytoplasm, where they subvert signaling pathways of the intestinal epithelium. Here, we report that the anti-apoptotic regulator HS1-associated protein X1 (HAX-1) is an interaction partner of the T3SS effectors EspO of enterohaemorrhagic Escherichia coli (EHEC) and Citrobacter rodentium, OspE of Shigella flexneri and Osp1STYM of Salmonella enterica serovar Typhimurium. EspO, OspE and Osp1STYM have previously been reported to interact with the focal adhesions protein integrin linked kinase (ILK). We found that EspO localizes both to the focal adhesions (ILK localization) and mitochondria (HAX-1 localization), and that increased expression of HAX-1 leads to enhanced mitochondrial localization of EspO. Ectopic expression of EspO, OspE and Osp1STYM protects cells from apoptosis induced by staurosporine and tunicamycin. Depleting cells of HAX-1 indicates that the anti-apoptotic activity of EspO is HAX-1 dependent. Both HAX-1 and ILK were further confirmed as EspO1 interacting proteins during infection using T3SS-delivered EspO1. Using cell detachment as a proxy for cell death we confirmed that T3SS-delivered EspO1 could inhibit cell death induced during EPEC infection, to a similar extent as the anti-apoptotic effector NleH, or treatment with the pan caspase inhibitor z-VAD. In contrast, in cells lacking HAX-1, EspO1 was no longer able to protect against cell detachment, while NleH1 and z-VAD maintained their protective activity. Therefore during both infection and ectopic expression EspO protects cells from cell death by interacting with HAX-1. These results suggest that despite the differences between EHEC, C. rodentium, Shigella and S. Typhimurium infections, hijacking HAX-1 anti-apoptotic signaling is a common strategy to maintain the viability of infected cells.

2021-10-15 | PXD023126 | Pride

VS94 SAPI AI-2 Temporal study

Project description:VS94 gene expression at different time-points in SAPI medium in absence and presence of AI-2 was studied. Autoinducer-2 (AI-2) is produced by many species of bacteria, including various commensal bacteria and is involved in inter-species communication. Since, pathogens encounter AI-2 once they enter the human gastro-intestinal tract; we studied the effects of presence of AI-2 on various phenotypes associated with infection and colonization of enterohemorrhagic Escherichia coli (EHEC) namely, chemotaxis, motility and attachment to HeLa cells. AI-2 attracted EHEC when observed in agarose plug assays and also increased EHEC motility by 1.44-fold. AI-2 also increased EHEC attachment to HeLa cells by 1.6-fold; hence, suggesting that exposure to AI-2 inside the gastro-intestinal tract can play an important role in EHEC colonization. We then investigated the global effects of AI-2 on EHEC gene expression using DNA microarrays at various time-points. We found that AI-2 controls virulence gene expression and several other groups of genes (flagellar genes, iron related genes, biofilm genes etc.) associated with virulence in a time-dependent manner. Hence, through these studies we have shown that AI-2 may be a key component in EHEC infection of human gastro-intestinal tract. Keywords: Time course

2008-03-21 | GSE9388 | GEO

Transcriptomic analysis for response of EHEC to short chain fatty acids

Project description:Enterohaemorrhagic Escherichia coli (EHEC) is an emerging pathogen that causes diarrhea and heamolytic uremic syndrome. Expression of genes associated to pathogenicity is strictly regulated by environmental factors. Since short chian fatty acids (SCFAs) are present in intestinal tract which is a target of EHEC infection, we investigated the response of EHEC genes to SCFAs, such as acetate, propionate and butyrate. Keywords: Culture condition

2008-11-01 | GSE12903 | GEO

The E. coli type III secreted effectors NleB and EspL interact with the microtubule associated protein ensconsin to disrupt vesicle trafficking, part 1

Project description:Enteropathogenic and enterohaemorrhagic E. coli (EPEC and EHEC) translocate a set of type III effector proteins into host cells that are critical for bacterial virulence. These effectors subvert normal host pathways by interacting with a variety of targets within the cell, but the binding partners and mechanism of action of the majority of effectors are not understood. We identified the microtubule associated protein, ensconsin, as a novel target for two EPEC/EHEC effectors. We found that the secreted effectors NleB and EspL bind host ensconsin and work synergistically to paralyze kinesin-based intracellular vesicular transport. Our findings demonstrate that EPEC/EHEC encode multiple effectors that control intracellular vesicle movement and suggest a simple strategy for broad-based immobilization of host cells by pathogens.

2016-12-22 | PXD002933 | Pride

Expression data from Stx2-treated human renal proximal tubular epithelial cell (RPTEC)

Project description:Shiga toxin type 2 (Stx2) from Escherichia coli is thought to be a main factor to casue renal dysfunction in Enterohemorrhagic E. coli (EHEC) infection. The renal dysfunction caused by the proximal tubular defects can be detected in the earlier EHEC infection. However, the precise information of gene expression from proximal tubular epithelial cells has yet to be clarified. We performed microarray experiments using Stx2-injected mouse kidney and Stx2-treated human renal proximal tubular epithelial cells (RPTEC), and extracted common genes that were differentially expressed.

2022-01-01 | GSE172466 | GEO

Expression data from Stx2-injected (i.p.) mouse kidneys

2022-01-01 | GSE172465 | GEO

Enteropathogenic Escherichia Coli (EPEC): Does it Have a Role in Colorectal Tumourigenesis?

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.

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