Identification of additional virulence determinants on the pYV plasmid of Yersinia enterocolitica W227

Mulder, Bert; Michiels, Thomas; Simonet, Michel; Sory, Marie‐Paule; Cornelis, Guy R.

doi:10.1128/iai.57.8.2534-2541.1989

Cited by 94 publications

(67 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As expected, several polypeptide bands detected in OMP profiles from IP383 grown at 37°C were absent in those from IP383 grown at 25°C and from IP383p-grown at 25°C or at 37°C. These polypeptides coincided with YOPs found in virulent 09 strains by several authors [1,18,19].…”

Section: Omp Profiles Of the Isogenic Strains Ip383 And Ip383p-supporting

confidence: 83%

Chromosome-mediated resistance of Yersinia enterocolitica serotype O9 to intracellular killing by mouse peritoneal macrophages

Ruiz‐Bravo

1994

FEMS Immunology and Medical Microbiology

View full text Add to dashboard Cite

The survival of Yersinia enterocolitica serotype O9 within mouse peritoneal macrophages was investigated. To evaluate the role of the virulence plasmid in the resistance to intracellular killing, an isogenic pair of virulent (plasmid-bearing) and avirulent (plasmid-less) O9 strains was used. The virulent strain was able to express plasmid-encoded outer membrane proteins and to colonize the Peyer's patches of orally infected mice. When mice were infected intraperitoneally, both strains were recovered at similar rates and over the same time from the peritoneal cavity. When in vitro assays were performed, both strains showed similar resistance to intracellular killing by monolayers of resident and inflammatory peritoneal macrophages. Previous opsonization of bacteria did not modify their survival within macrophage monolayers. We concluded that serotype O9 strains display a chromosome-mediated resistance to intracellular killing by mouse peritoneal macrophages. Moreover, macrophage resistance does not seem to be of importance for virulence of serotype O9 strains in mice.

show abstract

Section: Omp Profiles Of the Isogenic Strains Ip383 And Ip383p-supporting

confidence: 83%

Chromosome-mediated resistance of Yersinia enterocolitica serotype O9 to intracellular killing by mouse peritoneal macrophages

Ruiz‐Bravo

1994

FEMS Immunology and Medical Microbiology

View full text Add to dashboard Cite

show abstract

“…This YopM-mediated scaffolding results in activation of kinases downstream of the Yersinia YopJ block in the MAPK pathways (see below) (McDonald et al, 2003). Although the role of YopM in pathogenesis remains unclear, it is important in a mouse model of infection because of decreased virulence in mice infected with a YopM null strain (Mulder et al, 1989;Leung et al, 1990).…”

Section: Elucidating Mechanisms Of Yersinia Effectors 559mentioning

confidence: 99%

Yersinia outer proteins: Yops

2008

View full text Add to dashboard Cite

SummaryThe pathogenic bacteria Yersinia spp. contain a virulence plasmid that encodes a type III secretion system and effectors. During infection, four of the effectors target the actin cytoskeleton, crippling the phagocytic machinery in the infected cell. The remaining two effectors dampen the innate immune response by targeting important signalling pathways. Although the biochemical activity for each of these effectors is known, the mechanisms involved in their ordered secretion and delivery remain elusive.

show abstract

“…YopK (YopQ) is a 21 kDa secreted protein that is required for virulence in the pathogenic Yersinia species (Straley and Bowmer, 1986;Mulder et al, 1989;Straley and Cibull, 1989;Holmströ m et al, 1995). Although a yopK mutant of Y. pseudotuberculosis was found to be avirulent, it was still able to induce cytotoxicity in HeLa cells and to inhibit phagocytosis by the mouse-macrophage cell line J774 .…”

Section: Introductionmentioning

confidence: 99%

YopK of Yersinia pseudotuberculosis controls translocation of Yop effectors across the eukaryotic cell membrane

Holmström

Petterson

Rosqvist

et al. 1997

Molecular Microbiology

127

161

View full text Add to dashboard Cite

SummaryIntroduction of anti-host factors into eukaryotic cells by extracellular bacteria is a strategy evolved by several Gram-negative pathogens. In these pathogens, the transport of virulence proteins across the bacterial membranes is governed by closely related type III secretion systems. For pathogenic Yersinia, the protein transport across the eukaryotic cell membrane occurs by a polarized mechanism requiring two secreted proteins, YopB and YopD. YopB was recently shown to induce the formation of a pore in the eukaryotic cell membrane, and through this pore, translocation of Yop effectors is believed to occur (Hå kansson et al., 1996b). We have previously shown that YopK of Yersinia pseudotuberculosis is required for the development of a systemic infection in mice. Here, we have analysed the role of YopK in the virulence process in more detail. A yopK-mutant strain was found to induce a more rapid YopE-mediated cytotoxic response in HeLa cells as well as in MDCK-1 cells compared to the wild-type strain. We found that this was the result of a cell-contact-dependent increase in translocation of YopE into HeLa cells. In contrast, overexpression of YopK resulted in impaired translocation. In addition, we found that YopK also influenced the YopBdependent lytic effect on sheep erythrocytes as well as on HeLa cells. A yopK-mutant strain showed a higher lytic activity and the induced pore was larger

show abstract

Identification of additional virulence determinants on the pYV plasmid of Yersinia enterocolitica W227

Cited by 94 publications

References 36 publications

Chromosome-mediated resistance of Yersinia enterocolitica serotype O9 to intracellular killing by mouse peritoneal macrophages

Chromosome-mediated resistance of Yersinia enterocolitica serotype O9 to intracellular killing by mouse peritoneal macrophages

Yersinia outer proteins: Yops

YopK of Yersinia pseudotuberculosis controls translocation of Yop effectors across the eukaryotic cell membrane

Contact Info

Product

Resources

About