Contribution of the Major Secreted Yops of
            <i>Yersinia enterocolitica</i>
            O:8 to Pathogenicity in the Mouse Infection Model

Trülzsch, Konrad; Sporleder, Thorsten; Igwe, Emeka I.; Rüssmann, Holger; Heesemann, Jürgen

doi:10.1128/iai.72.9.5227-5234.2004

Cited by 145 publications

(167 citation statements)

References 63 publications

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“…The immune response to bacteria depends to a large extent on the degree of colonization of the host (colonization of Peyer's patches only vs colonization of liver/spleen). This might account for the poor CD8 T cell response after infection of mice with the yopH, yopM, and yopQ mutants, which are highly attenuated and able to colonize only the gut and Peyer's patches (57). However, because the yopE mutant is comparable in virulence to the yopP mutant (57) differences in colonization are not likely to have influenced this result.…”

Section: Discussionmentioning

confidence: 74%

“…Previously we demonstrated that a yopP knockout mutant of Y. enterocolitica was attenuated in an oral mouse infection model (57). In contrast to mice infected with the WA-C(pYV) strain, mice infected with the yopP mutant were able to control infection, eliminating bacteria from spleens and livers by day 12 postinfection.…”

Section: Discussionmentioning

confidence: 99%

“…WA-C(pYV) (57) harbors a chloramphenicol cassette in a noncoding region of the pYV plasmid and is as virulent as WA-314 (57). WA-C(pYV⌬P) and WA-C(pYV⌬E) are isogenic yopP and yopE deletion mutants, respectively, that were previously described (57). WA-C(pYV-515) harbors a TN5 insertion in low calcium response gene lcrD and is deficient in translocation of all Yops (58).…”

Section: Bacterial Strains and Plasmidsmentioning

confidence: 99%

“…Transcription of the gene fusion and sycE is mediated by the wild-type yopE/sycE promoter. Plasmid pHR430 was transformed into parental WA-C(pYV) as well as the previously described yopP and yopE mutants WA-C(pYV⌬P) and WA-C(pYV⌬E), respectively (57).…”

Section: Yopp Inhibits Cd8 T Cell Response In Vivomentioning

confidence: 99%

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Yersinia Outer Protein P Inhibits CD8 T Cell Priming in the Mouse Infection Model

Trülzsch

Geginat²,

Sporleder

et al. 2005

The Journal of Immunology

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Pathogenic yersiniae translocate a mixture of effector proteins called Yersinia outer proteins (Yops) into the cytosol of eukaryotic cells by their type III secretion system. YopP is one of the best characterized of these effector proteins and known to inhibit the proinflammatory response of the host by interfering with NF-κB signal transduction and inducing apoptosis of macrophages. The effects of YopP on the immune response were studied by a Yersinia Ag-independent approach using bacteria that translocate the well-characterized model Ag listeriolysin O of Listeria monocytogenes via their type III secretion system. In this study we demonstrate a novel function for YopP in vivo. It is shown for the first time that YopP not only counteracts the innate immune defense but also inhibits the adaptive immune system by suppressing the development of an effective CD8 T cell response in a mouse model. A possible mechanism for this could be the inhibition of Ag presentation by dendritic cells (DC). In vitro this is shown to be due to the rapid induction of programmed DC death and to inhibition of DC maturation. Using this approach we could further show that the listeriolysin O-specific CD8 T cells generated in vivo by the yopP mutant are functional and are able to protect mice against a lethal challenge with wild type Listeria.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Section: Bacterial Strains and Plasmidsmentioning

confidence: 99%

Section: Yopp Inhibits Cd8 T Cell Response In Vivomentioning

confidence: 99%

See 2 more Smart Citations

Yersinia Outer Protein P Inhibits CD8 T Cell Priming in the Mouse Infection Model

Trülzsch

Geginat²,

Sporleder

et al. 2005

The Journal of Immunology

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“…This could finally contribute to determine the progression of Yersinia infection in the compromised host. It has been revealed that YopE is required for prolonged colonization of Y. enterocolitica-infected mice (55). This suggests that the cellular effects conferred by YopE primarily play a role in maintaining persistent Yersinia infection, rather than in triggering acute overwhelming disease.…”

Section: Discussionmentioning

confidence: 99%

The Proteasome Pathway Destabilizes Yersinia Outer Protein E and Represses Its Antihost Cell Activities

Ruckdeschel

Pfaffinger

Trülzsch

et al. 2006

The Journal of Immunology

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Pathogenic Yersinia spp. neutralize host defense mechanisms by engaging a type III protein secretion system that translocates several Yersinia outer proteins (Yops) into the host cell. Although the modulation of the cellular responses by individual Yops has been intensively studied, little is known about the fate of the translocated Yops inside the cell. In this study, we investigated involvement of the proteasome, the major nonlysosomal proteolytic system in eukaryotic cells, in Yop destabilization and repression. Our data show that inhibition of the proteasome in Yersinia enterocolitica-infected cells selectively stabilized the level of YopE, but not of YopH or YopP. In addition, YopE was found to be modified by ubiquitination. This suggests that the cytotoxin YopE is physiologically subjected to degradation via the ubiquitin-proteasome pathway inside the host cell. Importantly, the increased levels of YopE upon proteasome inhibition were associated with decreased activity of its cellular target Rac. Thus, the GTPase-down-regulating function of YopE is enhanced when the proteasome is inhibited. The stabilization of YopE by proteasome inhibitor treatment furthermore led to aggravation of the cytotoxic YopE effects on the actin cytoskeleton and on host cell morphology. Together, these data show that the host cell proteasome functions to destabilize and inactivate the Yersinia effector protein YopE. This implies the proteasome as integral part of the cellular host immune response against the immunomodulatory activities of a translocated bacterial virulence protein.

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Recombineering in Non‐Model Bacteria

Corts¹,

Thomason

Costantino

et al. 2022

Current Protocols

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The technology of recombineering, in vivo genetic engineering, was initially developed in Escherichia coli and uses bacteriophage‐encoded homologous recombination proteins to efficiently recombine DNA at short homologies (35 to 50 nt). Because the technology is homology driven, genomic DNA can be modified precisely and independently of restriction site location. Recombineering uses linear DNA substrates that are introduced into the cell by electroporation; these can be PCR products, synthetic double‐strand DNA (dsDNA), or single‐strand DNA (ssDNA). Here we describe the applications, challenges, and factors affecting ssDNA and dsDNA recombineering in a variety of non‐model bacteria, both Gram‐negative and ‐positive, and recent breakthroughs in the field. We list different microbes in which the widely used phage λ Red and Rac RecET recombination systems have been used for in vivo genetic engineering. New homologous ssDNA and dsDNA recombineering systems isolated from non‐model bacteria are also described. The Basic Protocol outlines a method for ssDNA recombineering in the non‐model species of Shewanella. The Alternate Protocol describes the use of CRISPR/Cas as a counter‐selection system in conjunction with recombineering to enhance recovery of recombinants. We provide additional background information, pertinent considerations for experimental design, and parameters critical for success. The design of ssDNA oligonucleotides (oligos) and various internet‐based tools for oligo selection from genome sequences are also described, as is the use of oligo‐mediated recombination. This simple form of genome editing uses only ssDNA oligo(s) and does not require an exogenous recombination system. The information presented here should help researchers identify a recombineering system suitable for their microbe(s) of interest. If no system has been characterized for a specific microbe, researchers can find guidance in developing a recombineering system from scratch. We provide a flowchart of decision‐making paths for strategically applying annealase‐dependent or oligo‐mediated recombination in non‐model and undomesticated bacteria. © 2022 Wiley Periodicals LLC. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA. Basic Protocol: ssDNA recombineering in Shewanella species Alternate Protocol: ssDNA recombineering coupled to CRISPR/Cas9 in Shewanella species

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Contribution of the Major Secreted Yops of Yersinia enterocolitica O:8 to Pathogenicity in the Mouse Infection Model

Cited by 145 publications

References 63 publications

Yersinia Outer Protein P Inhibits CD8 T Cell Priming in the Mouse Infection Model

Yersinia Outer Protein P Inhibits CD8 T Cell Priming in the Mouse Infection Model

The Proteasome Pathway Destabilizes Yersinia Outer Protein E and Represses Its Antihost Cell Activities

Recombineering in Non‐Model Bacteria

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