Yersinia pseudotuberculosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA16072 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| DRR287732_1.fastq.gz | Fastqsanger.gz | |||
| DRR287733_1.fastq.gz | Fastqsanger.gz | |||
| DRR287733_2.fastq.gz | Fastqsanger.gz | |||
| DRR505511_subreads.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Yersinia pseudotuberculosis is a Gram-negative bacterium capable of causing gastrointestinal infection and is closely related to the highly virulent plague bacillus Yersinia pestis. Infection by both species are currently treatable with antibiotics such as ciprofloxacin, a quinolone-class drug of major clinical importance in the treatment of many other infections. Our current understanding of the mechanism of action of ciprofloxacin is that it inhibits DNA replication by targeting DNA gyrase, and that resistance is primarily due to mutation at this target site, along with generic efflux and detoxification strategies. We utilised transposon directed insertion site sequencing (TraDIS or TnSeq) to identify the non-essential chromosomal genes in Y. pseudotuberculosis that are required to tolerate sub-lethal concentrations of ciprofloxacin in vitro. As well as highlighting recognised antibiotic resistance genes, we provide evidence that a multitude of genes involved in regulating DNA replication and repair are central in enabling Y. pseudotuberculosis to tolerate the antibiotic, including dksA (yptb0734), a regulator of RNA polymerase and hda (yptb2792), an inhibitor of DNA replication initiation. We furthermore demonstrate that even at sub-lethal concentrations, ciprofloxacin causes severe cell-wall stress, requiring lipopolysaccharide lipid A, O-antigen and core biosynthesis genes to resist the sub-lethal effects of the antibiotic. It is evident that coping with the consequence(s) of antibiotic-induced stress requires the contribution of scores of genes that are not exclusively engaged in drug-resistance.
2019-08-02 | GSE135236 | GEO
Project description:Neutrophils are essential components of immunity and are rapidly recruited to infected or injured tissue. Upon their activation, neutrophils release granules to the cell's exterior, through a process called degranulation. These granules contain proteins with antimicrobial properties that help combat infection. The enteropathogenic bacterium Yersinia pseudotuberculosis successfully persists as an extracellular bacterium during infection by virtue of its translocation of virulence effectors (Yersinia outer proteins [Yops]) that act in the cytosol of host immune cells to subvert phagocytosis and proinflammatory responses. Here, we investigated the effect of Y. pseudotuberculosis on neutrophil degranulation upon cell contact. We found that virulent Y. pseudotuberculosis was able to prevent secondary granule release. The blocking effect was general, as the release of primary and tertiary granules was also reduced. Degranulation of secondary granules was also blocked in primed neutrophils, suggesting that this mechanism could be an important element of immune evasion. Further, wild-type bacteria conferred a transient block on neutrophils that prevented their degranulation upon contact with plasmid-cured, avirulent Y. pseudotuberculosis and Escherichia coli Detailed analyses showed that the block was strictly dependent on the cooperative actions of the two antiphagocytic effectors, YopE and YopH, suggesting that the neutrophil target structures constituting signaling molecules needed to initiate both phagocytosis and general degranulation. Thus, via these virulence effectors, Yersinia can impair several mechanisms of the neutrophil's antimicrobial arsenal, which underscores the power of its virulence effector machinery.
| S-EPMC5116715 | biostudies-literature
Project description:Two cases of community-acquired septicemia caused by serotype-O1 Yersinia pseudotuberculosis were diagnosed in middle-aged, HIV-positive, immunodeficient patients during an 8-month period. Bacterial isolates were genetically indistinguishable, but no epidemiologic link between the 2 patients was established. HIV-related immunosuppression should be regarded as a risk factor for Y. pseudotuberculosis septicemia.
| S-EPMC3371805 | biostudies-literature
Project description:Pathogen that causes a tuberculosis-like infection of the lung
| PRJNA12950 | ENA
Project description:Gastrointestinal infections caused by enteric yersiniae can become persistent and complicated by relapsing enteritis and severe autoimmune disorders. To establish a persistent infection, the bacteria have to cope with hostile surroundings when they transmigrate through the intestinal epithelium and colonize underlying gut-associated lymphatic tissues. How the bacteria gain a foothold in the face of host immune responses is poorly understood. Here, we show that the CNFY toxin, which enhances translocation of the antiphagocytic Yop effectors, induces IL-6-triggered inflammatory responses. This results in extensive tissue destruction, alteration of the intestinal microbiota and bacterial clearance. An elimination of CNFY, however, increases inter-feron-γ-mediated responses, comprising non-inflammatory antimicrobial activities and Ido1-promoted tolerogenesis. This process is accompanied by a preterm reprogram-ming of the pathogen's transcriptional response towards persistence, which gives the bacteria a fitness edge against host responses. These results have significant implica-tions for our understanding how enteric bacteria establish a commensal-type life style.
2018-01-15 | GSE98802 | GEO