STEC new stx subtype
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB39088 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4297034.fastq.gz | Fastqsanger.gz | |||
| ERR4297035.fastq.gz | Fastqsanger.gz |
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Project description:The Escherichia coli strain Nissle 1917 (EcN) is used as a probiotic for the treatment of certain gastrointestinal diseases in several European and non-European countries. In vitro studies showed EcN to efficiently inhibit the production of Shiga toxin (Stx) by Stx producing E. coli (STEC) such as Enterohemorrhagic E. coli (EHEC). The occurrence of the latest EHEC serotype (O104:H4) responsible for the great outbreak in 2011 in Germany was due to the infection of an enteroaggregative E. coli by a Stx 2-encoding lambdoid phage turning this E. coli into a lysogenic and subsequently into a Stx producing strain. Since EHEC infected persons are not recommended to be treated with antibiotics, EcN might be an alternative medication. However, because a harmless E. coli strain might be converted into a Stx-producer after becoming host to a stx encoding prophage, we tested EcN for stx-phage genome integration. Our experiments revealed the resistance of EcN towards not only stx-phages but also against the lambda phage. This resistance was not based on the lack of or by mutated phage receptors. Rather the expression of certain genes (superinfection exclusion B (sieB) and a phage repressor (pr) gene) of a defective prophage of EcN was involved in the complete resistance of EcN to infection by the stx- and lambda phage. Obviously, EcN cannot be turned into a Stx producer. Furthermore, we observed EcN to inactivate phages and thereby to protect E. coli K-12 strains against infection by stx- as well as lambda-phages. Inactivation of lambda-phages was due to binding of lambda-phages to LamB of EcN whereas inactivation of stx-phages was caused by a thermostable protein of EcN. These properties together with its ability to inhibit Stx production make EcN a good candidate for the prevention of illness caused by EHEC and probably for the treatment of already infected people.
2018-06-14 | GSE109932 | GEO
Project description:Comparison of RNA expression profiles from STEC strain FHI96 expressing methyltransferase mod (ON; 52reps) or not (OFF; 51reps).
2024-06-30 | GSE129787 | GEO
Project description:Mice intraperitoneally administered with LPS and Stx exhibit HUS-like pathology. While mouse and human Gb3 localization is different, LPS and Stx induced kidney injury models in mice have been used to confirm responsiveness to various stx-related inflammatory pathways and treatments. In order for this mouse model to apply tHUS in humans, more detailed and exhaustive comprehension of this animal model is needed. Although molecular studies have been conducted on this mouse model before, we consider that there is still scope for further investigation of molecular pathways and studies on kidney damage segments. Overall, Biological pathways, upstream regulators, and downstream biological activities occurring in the kidney after LPS/Stx administration were identified through Ingenuity Pathway Analysis ™ using the result of microarray. In addition, we identified the detailed damaged site in the renal tubule from the down-regulation gene revealed by microarray.
2021-09-01 | GSE180476 | GEO
Project description:Loss of stx from Escherichia coli and Escherichia albertii
| PRJEB27634 | ENA
Project description:The Salmonella effector SteC is the only protein kinase encoded by Salmonella pathogenicity island 2 that is secreted through the type III secretion system. SteC is known to trigger actin rearrangement via the phosphorylated MEK pathway, and our previous experiments demonstrated that the migration process of macrophages found during Salmonella infection is dependent on the rearrangement of the host cell actin backbone and the action of SteC.To further investigate the target of SteC in the host, we constructed a SteC-RAW264.7 cell line and performed phosphomics analysis using 4D-FastDIA to identify the direct substrates of SteC that trigger macrophage migration and lead to cytoskeletal rearrangement.
2024-02-22 | PXD042038 | Pride
Project description:BACKGROUND AND OBJECTIVES:Shiga toxin-producing Escherichia coli (STEC) strains are human pathogens linked to hemorrhagic colitis and hemolytic uremic syndrome. Shiga toxins (Stx1 and Stx2) are the major virulence factors of these strains. The aim of this work was to study the prevalence and distribution of stx(1) and stx(2) gene in E. coli O157:H7 and non-O157:H7 strains isolated from cattle in Shiraz, Iran. MATERIALS AND METHODS:Four hundred and twenty samples consisted of recto-anal mucosal swabs were collected from cattle. They were checked for the presence of the stx1 and stx2 gene using multiplex-PCR every 1 week over a 1-year period (2007-2008). RESULTS:A total of 146 strains carrying the stx1 and stx2 gene were isolated from 51 (12.14%) cattle. Overall, 15 (3.57%) were identified as O157:H7 and 131 (31.19%) revealed to be non-O157:H7. Both stx2 and stx1 genes were detected in 51 (34.93%) STEC isolates. Genotypes stx1 and stx2 were detected in 15 (10.27%) and 78 (53.42%) respectively. Seasonal distribution of stx genes revealed high percentage of positive animals in warm seasons. The gene sequence similarity ranged from 94 to 100%. CONCLUSION:Frequency of stx1 and stx2 in animals and its relation to human disease is not well understood in Iran. The high prevalence of STEC in cattle seems to parallel that which is usually observed in warm seasons and it also parallels occurrence of human STEC. The higher prevalence of the stx2 gene than stx1 in strain populations isolated from cattle indicates a risk alert of E. coli O157:H7 being shed by cattle in these populations. Appropriate measures are now needed to prevent the spread of this life-threatening foodborne disease in our country.
| S-EPMC3279763 | biostudies-literature
Project description:To investigate the transcriptional changes caused by Stx1 and Stx2 in human kidney microvascular cells (HKMECs), and the effects of GCSi pre-treatment on Stx-mediated effects
2024-01-24 | GSE205723 | GEO
Project description:The identification of subtype-specific translocations has revolutionized diagnostics of sarcoma and provided new insight into oncogenesis. We used RNA-Seq to investigate samples diagnosed as small round cell tumors of bone, possibly Ewing sarcoma, but lacking the canonical EWSR1-ETS translocation. A new fusion was observed between the BCL6 co-repressor (BCOR) and the testis specific cyclin B3 (CCNB3) genes on chromosome X. RNA-Seq results were confirmed by RT-PCR and cloning the tumor-specific genomic translocation breakpoints. 24 BCOR-CCNB3-positive tumors were identified among a series of 594 sarcomas. Gene profiling experiments indicate that BCOR-CCNB3-positive cases are biologically distinct from other sarcomas, particularly EwingM-bM-^@M-^Ys sarcoma. Finally, we show that CCNB3 immunohistochemistry is a powerful diagnostic marker for this group of sarcoma and that over-expression of BCOR-CCNB3 or of a truncated CCNB3 activates S-phase in NIH3T3 cells. Thus the intrachromosomal X fusion described here represents a new subtype of bone sarcoma caused by a novel gene fusion mechanism. Comparison of expression profiles of 10 BCOR-CCNB3 samples (plus 4 EWS-FLI1 Ewing sarcomas samples as control) with publicly available profiles of other tumor types.
2012-03-03 | E-GEOD-34800 | biostudies-arrayexpress