Evidence map›Paper›PMID 24491574›Full record

ArticleInfection and immunity2014

PrtR homeostasis contributes to Pseudomonas aeruginosa pathogenesis and resistance against ciprofloxacin.

Ziyu Sun, Jing Shi, Chang Liu, Yongxin Jin, Kewei Li, Ronghao Chen, Shouguang Jin, Weihui Wu

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 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

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  2. Genomic Insights into the Pathogenicity of HypervirulentPathogens (Basel, Switzerland) · 2025
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  8. ECF Sigma Factor HxuI Is Critical forMicrobiology spectrum · 2022
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  9. MvaT negatively regulates pyocin S5 expression inBiotechnology notes (Amsterdam, Netherlands) · 2022
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  10. Sending out an SOS - the bacterial DNA damage response.Genetics and molecular biology · 2022
    Article
  11. Article
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  13. Review
  14. Article
  15. Article
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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

8 authors at 1 institution in 2 countries.

Ziyu SunKey Laboratory of Molecular Microbiology and Technology of the Ministry of Education, Department of Microbiology, College of Life Sciences, Nankai University, Tianjin, China.
Jing Shi
Chang Liu
Yongxin Jin
Kewei Li
Ronghao Chen
Shouguang Jin
Weihui Wu
Nankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudomonas aeruginosa is an opportunistic pathogen that causes acute and chronic infections in humans. Pyocins are bacteriocins produced by P. aeruginosa that are usually released through lysis of the producer strains. Expression of pyocin genes is negatively regulated by PrtR, which gets cleaved under SOS response, leading to upregulation of pyocin synthetic genes. Previously, we demonstrated that PrtR is required for the expression of type III secretion system (T3SS), which is an important virulence component of P. aeruginosa. In this study, we demonstrate that mutation in prtR results in reduced bacterial colonization in a mouse acute pneumonia model. Examination of bacterial and host cells in the bronchoalveolar lavage fluids from infected mice revealed that expression of PrtR is induced by reactive oxygen species (ROS) released by neutrophils. We further demonstrate that treatment with hydrogen peroxide or ciprofloxacin, known to induce the SOS response and pyocin production, resulted in an elevated PrtR mRNA level. Overexpression of PrtR by a tac promoter repressed the endogenous prtR promoter activity, and electrophoretic mobility shift assay revealed that PrtR binds to its own promoter, suggesting an autorepressive mechanism of regulation. A high level of PrtR expressed from a plasmid resulted in increased T3SS gene expression during infection and higher resistance against ciprofloxacin. Overall, our results suggest that the autorepression of PrtR contributes to the maintenance of a relatively stable level of PrtR, which is permissive to T3SS gene expression in the presence of ROS while increasing bacterial tolerance to stresses, such as ciprofloxacin, by limiting pyocin production.

Indexed as

Acute DiseaseAnimalsAnti-Bacterial AgentsBacterial ProteinsBiofilmsBronchoalveolar Lavage FluidCiprofloxacinDisease Models, AnimalDrug Resistance, BacterialFemaleGene Expression Regulation, BacterialHomeostasisHydrogen PeroxideMiceMice, Inbred BALB CMicrobial Sensitivity TestsAnti-Bacterial AgentsBacterial ProteinsCiprofloxacinHydrogen PeroxideprtR protein, Pseudomonas aeruginosaPyocinsReactive Oxygen SpeciesRepressor ProteinsRNA, Messenger

Identifiers

PMID24491574
PMCPMC3993409
OpenAlexW2156912526

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.