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Dynamic gene network analysis of Caco-2 cell response to Shiga toxin-producing Escherichia coli-associated hemolytic-uremic syndrome

ABSTRACT: Dynamic gene network analysis of Caco-2 cell response to Shiga toxin-producing Escherichia coli-associated hemolytic-uremic syndrome

PROVIDER: PRJNA412830 | ENA |

REPOSITORIES: ENA

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Dynamic Gene Network Analysis of Caco-2 Cell Response to Shiga Toxin-Producing Escherichia coli-Associated Hemolytic–Uremic Syndrome

Project description:Dynamic Gene Network Analysis of Caco-2 Cell Response to Shiga Toxin-Producing Escherichia coli-Associated Hemolytic–Uremic Syndrome

| PRJNA412855 | ENA

Dynamic Gene Network Analysis of Caco-2 Cell Response to Shiga Toxin-Producing Escherichia coli-Associated Hemolytic–Uremic Syndrome

Project description:Dynamic Gene Network Analysis of Caco-2 Cell Response to Shiga Toxin-Producing Escherichia coli-Associated Hemolytic–Uremic Syndrome

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Shiga toxin 2a induces mitochondrial damage, mitophagy and apoptosis via the interaction of Tom20 in Caco-2 cells

Project description:Shiga toxin type 2 (Stx2) is the main virulence factor produced by Stx-producing Escherichia coli (STEC) responsible for hemorrhagic colitis and the life-threatening sequela hemolytic uremic syndrome.

2022-11-21 | PXD038256 |

Effects of E. coli Shiga toxin on the gene expression profile of human microvascular endothelial cells

Project description:Changes in endothelial phenotype induced by E. coli-derived Shiga toxins (Stx) are believed to play a critical role in the pathogenesis of hemolytic uremic syndrome. Stx inactivate host ribosomes, but also alter gene expression at concentrations that minimally affect global protein synthesis. The effect of Stx on the gene expression profile of human microvascular endothelial cells was examined using the Affymetrix HG-U133A platform. Data were processed using 13 different methods and revealed 369 unique differentially expressed genes, 318 of which were up-regulated and 51 of which were down-regulated. These studies implicated activation of the CXCR4/CXCR7/SDF-1 chemokine pathway in Stx-mediated pathogenesis. Primary human dermal microvascular endothelial cells were treated with vehicle or Shiga toxin (10 fM, 24 h, n = 6) and changes in steady-state mRNA levels were determined by hybridization to Affymetrix HG-U133A arrays

2011-10-10 | E-GEOD-32710 | biostudies-arrayexpress

Alterations in gene expression in response to different regimes of Shiga toxin 2

Project description:The microarray data provided here belong to a study that describes two different Shiga toxin (Stx) induced models of hemolytic uremic syndrome (HUS) in mice. Although several rodent models of HUS were published, it still remains difficult to reproduce all clinical features of human HUS. Here, two different Stx2 regimes combined with volume resuscitation were tested in C57BL/6J wild type mice. Animals were euthanized because of kidney injury after 3 or 7 days respectively. Kidneys were removed for histological evaluation and RNA extraction. Kidney injury was confirmed histologically and by laboratory parameters in plasma. Data for the respective vehicle treated groups are also provided here.

2017-10-01 | GSE99229 | GEO

Dynamic Gene Network Analysis of Caco-2 Cell Response to Shiga Toxin-Producing Escherichia coli-Associated Hemolytic–Uremic Syndrome

Project description:A dynamic network approach was conducted to investigate the differential Caco-2 response to two STEC isolates - EH41, isolated from a HUS patient in Australia, and Ec472/01, isolated from bovine feces in Brazil - along in vitro enterocyte-bacteria interaction. The genomic analysis was based on temporal gene co-expression analysis (GCN) data in order to gain a better understanding on the molecular mechanisms underlying the capacity to cause HUS. The GCN topological analyses for Caco-2/EH41 group revealed loss of the scale-free status after one hour of interaction, persistence of this condition along the second hour and establishment of a new gene hierarchy thereafter. These events resemble the gene network mechanism of health-disease transition. The new established network represents an adaptive cell response to the pathogen and not the return to a “normal” state. Conversely, the networks for Caco-2/Ec472 group showed a slow and progressive loss of the scale-free status without its restoration at the end of the time interval here studied. These results contribute for a better understanding of the molecular mechanism involved in STEC pathogenicity associated to HUS.

2019-07-15 | GSE104489 | GEO

Dynamic Gene Network Analysis of Caco-2 Cell Response to Shiga Toxin-Producing Escherichia coli-Associated Hemolytic–Uremic Syndrome

2019-07-15 | GSE104488 | GEO

Tissue responses to Shiga toxin in human intestinal organoids

Project description:Intestinal tissue responses to protein synthesis inhibition by Shiga toxin are complex. Organoid models allow for an unprecedented examination of human tissue responses to a deadly Shiga toxin.

2020-02-01 | GSE144633 | GEO

Effects of E. coli Shiga toxin on the gene expression profile of human microvascular endothelial cells

2011-10-11 | GSE32710 | GEO

Shiga toxin remodels the intestinal epithelial transcriptional response to Enterohemorrhagic Escherichia coli

Project description:Enterohemorrhagic Escherichia coli (EHEC) is a food-borne pathogen that causes diarrheal disease and the potentially lethal hemolytic uremic syndrome. Here, we used an infant rabbit model of EHEC infection that recapitulates many aspects of human intestinal disease to comprehensively assess the host colonic epithelial and lamina propria cell transcriptional responses to EHEC infection. Furthermore, comparisons of colonic pathology and intestinal transcriptomic profiles in animals infected with EHEC strains containing or lacking Shiga toxins (∆∆stx) were carried out to investigate how these potent toxins shape the host response to the pathogen. We found that Stx is required for severe, multi-focal hemorrhage and extensive apoptosis in the colon. RNA-sequencing revealed that EHEC infection elicits a robust innate immune response in the colonic epithelium that is dramatically shaped by Stx. Over 1400 genes were differentially expressed in animals infected with WT versus ∆∆stx EHEC strains. Several pathways linked to innate immune responses were dependent on Stx. Upregulated genes in the presence of toxin included cytokines IL23a and CXCL8, as well as F3, the gene encoding the coagulation initiator Tissue Factor. RNA FISH revealed that these elevated transcripts were found almost exclusively in epithelial cells, suggesting that Stx remodels the transcriptional profile of the epithelium. Collectively, these findings reveal that Stx potently modulates the innate immune response to EHEC in the intestine, and suggest that Stx drives the response to infection towards type 3 immunity.

2021-01-14 | GSE156056 | GEO

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