Evidence map›Paper›PMID 20696867›Full record

ArticleAntimicrobial agents and chemotherapy2010

The development of ciprofloxacin resistance in Pseudomonas aeruginosa involves multiple response stages and multiple proteins.

Hsun-Cheng Su, Kevin Ramkissoon, Janet Doolittle, Martha Clark, Jainab Khatun, Ashley Secrest, Matthew C Wolfgang, Morgan C Giddings

Open access · greenAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.6field-weighted citation impact, top 38% 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

21 citing papers in PubMed, 49 citations in OpenAlex.

  1. Targeting biofilm and virulence inMicrobiology spectrum · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Adaptive response ofMicrobiology (Reading, England) · 2024
    Article
  7. Deferiprone-Gallium-Protoporphyrin Chitogel DecreasesMaterials (Basel, Switzerland) · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. The Role of Proteomics in Bacterial Response to Antibiotics.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

8 authors at 1 institution in 1 country.

Hsun-Cheng SuDepartment of Microbiology and Immunology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Kevin Ramkissoon
Janet Doolittle
Martha Clark
Jainab Khatun
Ashley Secrest
Matthew C Wolfgang
Morgan C Giddings
University of North Carolina at Chapel Hill · US

Funding

Software to Identify Post-translational Modifications From Proteomic Data SetsR01RR020823 · NCRR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI GIDDINGS, MORGAN CORINNE · 2004 to 2011
$2.6M
Cyclic AMP Signaling in Pseudomonas aeruginosa VirulenceR01AI069116 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WOLFGANG, MATTHEW C · 2008 to 2011
$1.3M
NCRR NIH HHS R01 RR020823NIAID NIH HHS AI069116NIAID NIH HHS R01 AI069116
6 · The paper itself

Abstract

Microbes have developed resistance to nearly every antibiotic, yet the steps leading to drug resistance remain unclear. Here we report a multistage process by which Pseudomonas aeruginosa acquires drug resistance following exposure to ciprofloxacin at levels ranging from 0.5× to 8× the initial MIC. In stage I, susceptible cells are killed en masse by the exposure. In stage II, a small, slow to nongrowing population survives antibiotic exposure that does not exhibit significantly increased resistance according to the MIC measure. In stage III, exhibited at 0.5× to 4× the MIC, a growing population emerges to reconstitute the population, and these cells display heritable increases in drug resistance of up to 50 times the original level. We studied the stage III cells by proteomic methods to uncover differences in the regulatory pathways that are involved in this phenotype, revealing upregulation of phosphorylation on two proteins, succinate-semialdehyde dehydrogenase (SSADH) and methylmalonate-semialdehyde dehydrogenase (MMSADH), and also revealing upregulation of a highly conserved protein of unknown function. Transposon disruption in the encoding genes for each of these targets substantially dampened the ability of cells to develop the stage III phenotype. Considering these results in combination with computational models of resistance and genomic sequencing results, we postulate that stage III heritable resistance develops from a combination of both genomic mutations and modulation of one or more preexisting cellular pathways.

Indexed as

Anti-Infective AgentsBacterial ProteinsCiprofloxacinDNA, BacterialDrug Resistance, BacterialElectrophoresis, Gel, Two-DimensionalMethylmalonate-Semialdehyde Dehydrogenase (Acylating)Microbial Sensitivity TestsPseudomonas aeruginosaSpectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationSuccinate-Semialdehyde DehydrogenaseAnti-Infective AgentsBacterial ProteinsCiprofloxacinDNA, BacterialMethylmalonate-Semialdehyde Dehydrogenase (Acylating)Succinate-Semialdehyde Dehydrogenase

Identifiers

PMID20696867
PMCPMC2976116
OpenAlexW2146073091

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.