Yersinia pseudotuberculosis PB1/+
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ABSTRACT:
PROVIDER: PRJNA28745 | ENA |
REPOSITORIES: ENA
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Project description:Yersinia pseudotuberculosis PB1/+ Genome sequencing
| PRJNA239343 | ENA
Project description:Yersinia pseudotuberculosis IB Genome sequencing
| PRJNA239357 | ENA
Project description:Serotype 1b strain isolated from a patient in Russia
| PRJNA16070 | ENA
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:Project goal is to identify proteomic profiles of Yersinia ruckeri, the causative agent of enteric redmouth disease in fish. Four strains (SP-05, CSF007-82, 7959-11 and YRNC-10) of Y. ruckeri were isolated from disease rainbow trout, Oncorhynchus mykiss. Strains, SP-05 and CSF007-82, belong to serotype 1 and biotype 1 (motile and lipase positive), while strains 7959-11 and YRNC-10 belong to serotype 1 and biotype 2 (non-motile and lipase negative) and belong to serotype 1. A single colony of each strain was inoculated into tryptic soy broth (Casein peptone, dipotassium hydrogen phosphate, glucose, sodium chloride, soya peptone, Sigma) and grown at 22 °C with shaking (150 rpm). These starter cultures were then diluted with fresh sterile tryptic soy broth to an optical density (OD 600) of 0.10 ± 0.05. Five hundred microlitres of the diluted starter cultures were inoculated in duplicates, into 25 ml of tryptic soy broth. Cultures were grown overnight at 22 °C with shaking (150 rpm) until the late log phase. Cells were harvested by centrifugation, then washed three times with PBS.
2017-09-22 | PXD005439 | Pride
Project description:Lipopolysaccharide (LPS), localized in the outer leaflet of the outer membrane, serves as the major surface component of the Gram-negative bacterial cell envelope responsible for the activation of the host's innate immune system. Variations of the LPS structure utilized by Gram-negative bacteria promote survival by providing resistance to components of the innate immune system and preventing recognition by TLR4. This review summarizes studies of the biosynthesis of Yersinia pseudotuberculosis complex LPSs, and the roles of their structural components in molecular mechanisms of yersiniae pathogenesis and immunogenesis.
| S-EPMC8533242 | biostudies-literature
Project description:Yersinia pestis, responsible for causing fulminant plague, has evolved clonally from the enteric pathogen, Y. pseudotuberculosis, which in contrast, causes a relatively benign enteric illness. An ~97% nucleotide identity over 75% of their shared protein coding genes is maintained between these two pathogens, leaving much conjecture regarding the molecular determinants responsible for producing these vastly different disease etiologies, host preferences and transmission routes. One idea is that coordinated production of distinct factors required for host adaptation and virulence in response to specific environmental cues could contribute to the distinct pathogenicity distinguishing these two species. Small non-coding RNAs that direct posttranscriptional regulation have recently been identified as key molecules that may provide such timeous expression of appropriate disease enabling factors. Here the burgeoning field of small non-coding regulatory RNAs in Yersinia pathogenesis is reviewed from the viewpoint of adaptive colonization, virulence and divergent evolution of these pathogens.
| S-EPMC4585118 | biostudies-literature