Ontology highlight
ABSTRACT:
PROVIDER: PRJNA578858 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Canine keratinocyte cell line (CPEK, CELLnTEC Advanced Cell Systems, Bern, Switzerland) : Unstimulated control (UC) vs. Samples stimulated by 4µg/mL recombinant human periostin (PO) (R&D Systems, Minneapolis, MN) for 6 or 24 hrs.
2017-01-20 | GSE77041 | GEO
Project description:C. difficile Ribotype 027 Outbreak in Bern, Switzerland
| PRJEB37809 | ENA
Project description:Human adenoviruses (HAdV) associated with pediatric patients in Bern, Switzerland
| PRJEB40708 | ENA
Project description:Rare human enterovirus genotypes in clinical respiratory samples in Bern, Switzerland
| PRJEB51320 | ENA
Project description:"Shigella spp. are the causative agents of shigellosis, which remains a major cause of death in children under the age of five. Shigellosis is marked by fever and leads to hemorrhagic diarrhea; Shigella bacteremia are reported in more severe cases. These clinical features strongly suggest that Shigella survive to plasma exposure, although it has not been previously investigated at a molecular level. In this report, we confirmed in a guinea pig model of shigellosis that local hemorrhages were induced by S. flexneri 5a and S. sonnei and we demonstrated that Shigella reached CD31+/CD34+ blood vessels within the mucosa during late infection stage and further disseminated in the blood circulation. These results confirmed the exposition of Shigella to plasma components during its virulence cycle, from the hemorrhagic colonic mucosa to the blood circulation. We demonstrated that all tested Shigella strains survived to plasma exposure in vitro and we have shown that Serine Protease Autrotransporters of Enterobacteriaceae (SPATEs) are essential for Shigella dissemination within the colonic mucosa and in the blood circulation. We confirmed that SPATEs were expressed and secreted within poorly oxygenated environments encountered by Shigella from hypoxic foci of infection to the blood circulation. We have further demonstrated that SPATEs promoted the survival of Shigella to plasma exposure, by cleaving the complement 3 component (C3), hence impairing the complement system activation."
2024-08-27 | PXD048033 | Pride
Project description:This study is an analysis of the Bern perioperative Biobank, a prospective cohort of adults who underwent cardiac surgery with the use of cardiopulmonary bypass at Bern University Hospital between January and December 2019. Blood samples were taken at induction of anaesthesia and on postoperative day one.
2023-11-27 | PXD046496 | Pride
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