Evidence map›Paper›PMID 18483548›Full record

ArticlePLoS pathogens2008

Reduced secretion of YopJ by Yersinia limits in vivo cell death but enhances bacterial virulence.

Igor E Brodsky, Ruslan Medzhitov

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Translocation of YopJ family effector proteins through the VirB/VirD4 T4SS ofProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Heightened Virulence ofInfection and immunity · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. The interplay between regulated necrosis and bacterial infection.Cellular and molecular life sciences : CMLS · 2016
    Review
  16. Article
  17. Article
  18. Yersinia type III effectors perturb host innate immune responses.World journal of biological chemistry · 2016
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Igor E BrodskyHoward Hughes Medical Institute and Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, United States of America. igor.brodsky@yale.edu
Ruslan Medzhitov
Howard Hughes Medical Institute · US

Funding

Treatments for Nipah Virus InfectionU54AI057159 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI FINBERG, ROBERT WILLIAM · 2003 to 2013
$113.7M
Interaction of Yersinia with dendritic cellsF32AI065081 · NIAID · YALE UNIVERSITY · PI BRODSKY, IGOR E · 2005 to 2007
$143k
Howard Hughes Medical InstituteNIAID NIH HHS 1 F32 AI065081NIAID NIH HHS F32 AI065081NIAID NIH HHS U54 AI057159
6 · The paper itself

Abstract

Numerous microbial pathogens modulate or interfere with cell death pathways in cultured cells. However, the precise role of host cell death during in vivo infection remains poorly understood. Macrophages infected by pathogenic species of Yersinia typically undergo an apoptotic cell death. This is due to the activity of a Type III secreted effector protein, designated YopJ in Y. pseudotuberculosis and Y. pestis, and YopP in the closely related Y. enterocolitica. It has recently been reported that Y. enterocolitica YopP shows intrinsically greater capacity for being secreted than Y. pestis YopJ, and that this correlates with enhanced cytotoxicity observed for high virulence serotypes of Y. enterocolitica. The enzymatic activity and secretory capacity of YopP from different Y. enterocolitica serotypes have been shown to be variable. However, the underlying basis for differential secretion of YopJ/YopP, and whether reduced secretion of YopJ by Y. pestis plays a role in pathogenesis during in vivo infection, is not currently known. It has also been reported that similar to macrophages, Y. enterocolitica infection of dendritic cells leads to YopP-dependent cell death. We demonstrate here that in contrast to Y. enterocolitica, Y. pseudotuberculosis infection of bone marrow-derived dendritic cells does not lead to increased cell death. However, death of Y. pseudotuberculosis-infected dendritic cells is enhanced by ectopic expression of YopP in place of YopJ. We further show that polymorphisms at the N-terminus of the YopP/YopJ proteins are responsible for their differential secretion, translocation, and consequent cytotoxicity. Mutation of two amino acids in YopJ markedly enhanced both translocation and cytotoxicity. Surprisingly, expression of YopP or a hypersecreted mutant of YopJ in Y. pseudotuberculosis resulted in its attenuation in oral mouse infection. Complete absence of YopJ also resulted in attenuation of virulence, in accordance with previous observations. These findings suggest that control of cytotoxicity is an important virulence property for Y. pseudotuberculosis, and that intermediate levels of YopJ-mediated cytotoxicity are necessary for maximal systemic virulence of this bacterial pathogen.

Indexed as

Host-Pathogen InteractionsAnimalsApoptosisBacterial ProteinsBone Marrow CellsCells, CulturedCytotoxicity Tests, ImmunologicDendritic CellsDisease Models, AnimalFemaleMacrophagesMiceMice, Inbred C57BLMutationPlasmidsPolymorphism, GeneticBacterial ProteinsYopP protein, Yersinia

Identifiers

PMID18483548
PMCPMC2361194
OpenAlexW2034561711

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.