Evidence map›Paper›PMID 24379284›Full record

ArticleInfection and immunity2014

Requirement of the Pseudomonas aeruginosa CbrA sensor kinase for full virulence in a murine acute lung infection model.

Amy T Y Yeung, Laure Janot, Olga M Pena, Anke Neidig, Irena Kukavica-Ibrulj, Ashley Hilchie, Roger C Levesque, Joerg Overhage, Robert E W Hancock

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 30% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Structure and conformational dynamics of the Pseudomonas CbrA transceptor.Protein science : a publication of the Protein Society · 2026
    Article
  3. Microbiology spectrum · 2026
    Article
  4. Article
  5. Structure and conformational dynamics of thebioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Role of Two-Component System Networks in Pseudomonas aeruginosa Pathogenesis.Advances in experimental medicine and biology · 2022
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Catabolism of Nucleic Acids by a Cystic FibrosisFrontiers in microbiology · 2019
    Article
  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

9 authors at 3 institutions in 2 countries.

Amy T Y YeungCentre for Microbial Diseases and Immunity Research, University of British Columbia, Vancouver, BC, Canada.
Laure Janot
Olga M Pena
Anke Neidig
Irena Kukavica-Ibrulj
Ashley Hilchie
Roger C Levesque
Joerg Overhage
Robert E W Hancock
University of British Columbia · CAKarlsruhe Institute of Technology · DEUniversité Laval · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Pseudomonas aeruginosa is an opportunistic pathogen that is a major cause of respiratory tract and other nosocomial infections. The sensor kinase CbrA is a central regulator of carbon and nitrogen metabolism and in vitro also regulates virulence-related processes in P. aeruginosa. Here, we investigated the role of CbrA in two murine models of infection. In both peritoneal infections in leukopenic mice and lung infection models, the cbrA mutant was less virulent since substantially larger numbers of cbrA mutant bacteria were required to cause the same level of infection as wild-type or complemented bacteria. In contrast, in the chronic rat lung model the cbrA mutant grew and persisted as well as the wild type, indicating that the decrease of in vivo virulence of the cbrA mutant did not result from growth deficiencies on particular carbon substrates observed in vitro. In addition, a mutant in the cognate response regulator CbrB showed no defect in virulence in the peritoneal infection model, ruling out the involvement of certain alterations of virulence properties in the cbrA mutant including defective swarming motility, increased biofilm formation, and cytotoxicity, since these alterations are controlled through CbrB. Further investigations indicated that the mutant was more susceptible to uptake by phagocytes in vitro, resulting in greater overall bacterial killing. Consistent with the virulence defect, it took a smaller number of Dictyostelium discoideum amoebae to kill the cbrA mutant than to kill the wild type. Transcriptional analysis of the cbrA mutant during D. discoideum infection led to the conclusion that CbrA played an important role in the iron metabolism, protection of P. aeruginosa against oxidative stress, and the regulation of certain virulence factors.

Indexed as

AnimalsBacterial ProteinsDictyosteliumFemaleHumansLungMacrophagesMaleMiceMice, Inbred C57BLMutationNeutrophilsPhagocytesPseudomonas aeruginosaPseudomonas InfectionsRatsBacterial ProteinsCbrA protein, Pseudomonas aeruginosaTranscription FactorsVirulence Factors

Identifiers

PMID24379284
PMCPMC3957987
OpenAlexW2164982854

What OpenQuestion holds

Textmetadata
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.