Ontology highlight
ABSTRACT:
PROVIDER: PRJNA705791 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Study of the foodborne Vibrio cholerae isolates from China
| PRJNA687920 | ENA
Project description:It was found that Vibrio splendidus could survive under high concentration of tetracycline, and the coelomic fluid of sea cucumber increased the tolerance of Vibrio splendidus to tetracycline. Therefore, the transcriptome was determined to find the cause of drug resistance in Vibrio splendidus.
2023-04-05 | GSE217630 | GEO
Project description:Transcriptional profiling of mycobacterium tuberculosis clinical isolates in China comparing extensively drug-resistant tuberculosis with drug sensitive one.
2009-04-04 | GSE15540 | GEO
Project description:Infections caused by carbapenem-resistant Acinetobacter baumannii (CRAb) are associated with high patient morbidity and mortality. The serious threat for human health imposed by CRAb was recently underscored by identification of close-to-untouchable carbapenem- and tetracycline-resistant isolates. Since outer membrane vesicles (OMVs) of Gram-negative bacteria may contribute to antimicrobial resistance, our present study was aimed at investigating OMVs produced by the first two carbapenem- and tetracycline-resistant CRAb isolates in Europe. These isolates, denoted CRAb1 and CRAb2 contain large, nearly identical plasmids that specify multiple resistances. Both isolates produce OMVs that were analyzed by differential light scattering, transmission electron microscopy and proteomics. By comparison with OMVs from the plasmid-free non-carbapenem-resistant A. baumannii isolate Ab1, which is an isogenic ancestor of the CRAb1 isolate, we show that plasmid carriage by the CRAb1 and CRAb2 isolates leads to an increased OMV size that is accompanied by increased diversity of the OMV proteome. Our analyses show that OMVs from CRAb1 and CRAb2 are major reservoirs of proteins involved in antimicrobial resistance, including the plasmid-encoded carbapenemases BlaNDM-1, and BlaOXA-97. We also show that these OMV-borne carbapenemases hydrolyze imipenem and protect otherwise carbapenem-sensitive A. baumannii and Escherichia coli isolates against this antibiotic. Altogether, our observations show that OMVs from highly drug-resistant CRAb confer tolerance against last-resort antibiotics to non-resistant bacterial pathogens.
2025-04-14 | PXD051698 | Pride
Project description:Transcriptional profiling of mycobacterium tuberculosis clinical isolates in China comparing extensively drug-resistant tuberculosis with drug sensitive one. The same condition experiment. The samples were from the different drug-resistant strains. Only one replicate.
2009-04-04 | E-GEOD-15540 | biostudies-arrayexpress
Project description:The study aimed to characterize plasmids mediating carbepenem resistance in Klebsiella pneumoniae in Pretoria, South Africa. We analysed 56 K. pneumoniae isolates collected from academic hospital around Pretoria. Based on phenotypic and molecular results of these isolates, 6 representative isolates were chosen for further analysis using long reads sequencing platform. We observed multidrug resistant phenotype in all these isolates, including resistance to aminoglycosides, tetracycline, phenicol, fosfomycin, floroquinolones, and beta-lactams antibiotics. The blaOXA-48/181 and blaNDM-1/7 were manily the plasmid-mediated carbapenemases responsible for carbapenem resistance in the K. pneumoniae isolates in these academic hospitals. These carbapenemase genes were mainly associated with plasmid replicon groups IncF, IncL/M, IncA/C, and IncX3. This study showed plasmid-mediated carbapenemase spread of blaOXA and blaNDM genes mediated by conjugative plasmids in Pretoria hospitals.
2019-10-17 | GSE138949 | GEO
Project description:Vibrio vulnificus causes severe necrotizing wound infections and life-threatening foodborne infections. While clinical isolates of V. vulnificus are well-established as human pathogens, the pathogenic mechanisms underlying the virulence of food-derived isolates, particularly in the case of wound infections, remain poorly understood. This study aimed to elucidate the pathogenic mechanisms of a highly virulent, seafood-derived V. vulnificus isolate. A molecular survey of 28 V. vulnificus isolates from Shenzhen identified four MARTX toxin types, with the D-type predominating (36%). We characterized a representative shrimp-derived isolate, Vv3, which carries a chromosomal D-type MARTX with an ACD-MCF-ABH-MCF effector architecture. Using a newly established mouse wound infection model, Vv3 induced 100% mortality within 12 hours, with high bacterial loads detected systemically. Pathological analysis revealed severe tissue damage at the infection site, marked by muscle necrosis, and significant distal organ damage. Strikingly, flow cytometry analysis of splenocytes showed a significant depletion of macrophages and lymphocytes, rather than a classic cytokine storm, which was supported by transcriptomic data. To dissect the molecular drivers underlying the pathogenicity of food-derived V. vulnificus, we generated isogenic toxin mutants. In vitro assays demonstrated that the MARTX toxin was the primary mediator of rapid cell death in both macrophages and epithelial cells. Deletion of the GD-rich repeat domain in the MARTX toxin (ΔrtxA-GD) significantly reduced cytotoxicity and allowed cells to maintain their morphology, while deletion of hemolysin (ΔvvhA) had a minor effect. Critically, In vivo mice wound infections indicated that MARTX-deficient mutants with or without deletion of vvhA is unable to cause mortality in mice. These results establish that the D-type MARTX toxin is the dominant virulence determinant in this foodborne isolate, driving mortality through a direct destruction of host cells. This study highlights the severe risk posed by foodborne V. vulnificus in wound exposures and informs that the GD-rich region serves as a potential target for intervention against V. vulnificus infection.
2025-09-22 | GSE308195 | GEO