Evidence map›Paper›PMID 29750823›Full record

ArticlePloS one2018

Resistance to pentamidine is mediated by AdeAB, regulated by AdeRS, and influenced by growth conditions in Acinetobacter baumannii ATCC 17978.

Felise G Adams, Uwe H Stroeher, Karl A Hassan, Shashikanth Marri, Melissa H Brown

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 19% 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, 37 citations in OpenAlex.

  1. Article
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  6. Alteration ofMicrobiology spectrum · 2023
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  9. RND pumps across the genusMicrobial genomics · 2023
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  10. Deciphering the virulence factors, regulation, and immune response toFrontiers in cellular and infection microbiology · 2023
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Update on Multidrug Resistance Efflux Pumps in Acinetobacter spp.Antimicrobial agents and chemotherapy · 2021
    Article
  16. Article
  17. TheFrontiers in microbiology · 2021
    Article
  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

5 authors at 2 institutions in 1 country.

Felise G AdamsCollege of Science and Engineering, Flinders University, Adelaide, SA, Australia.
Uwe H StroeherCollege of Science and Engineering, Flinders University, Adelaide, SA, Australia.
Karl A HassanDepartment of Chemistry and Biomolecular Sciences, Macquarie University, Sydney, NSW, Australia.
Shashikanth MarriCollege of Medicine and Public Health, Flinders University, Adelaide, SA, Australia.
Melissa H BrownCollege of Science and Engineering, Flinders University, Adelaide, SA, Australia.ORCID 0000-0001-6461-7550
Flinders University · AUMacquarie University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In recent years, effective treatment of infections caused by Acinetobacter baumannii has become challenging due to the ability of the bacterium to acquire or up-regulate antimicrobial resistance determinants. Two component signal transduction systems are known to regulate expression of virulence factors including multidrug efflux pumps. Here, we investigated the role of the AdeRS two component signal transduction system in regulating the AdeAB efflux system, determined whether AdeA and/or AdeB can individually confer antimicrobial resistance, and explored the interplay between pentamidine resistance and growth conditions in A. baumannii ATCC 17978. Results identified that deletion of adeRS affected resistance towards chlorhexidine and 4',6-diamidino-2-phenylindole dihydrochloride, two previously defined AdeABC substrates, and also identified an 8-fold decrease in resistance to pentamidine. Examination of ΔadeA, ΔadeB and ΔadeAB cells augmented results seen for ΔadeRS and identified a set of dicationic AdeAB substrates. RNA-sequencing of ΔadeRS revealed transcription of 290 genes were ≥2-fold altered compared to the wildtype. Pentamidine shock significantly increased adeA expression in the wildtype, but decreased it in ΔadeRS, implying that AdeRS activates adeAB transcription in ATCC 17978. Investigation under multiple growth conditions, including the use of Biolog phenotypic microarrays, revealed resistance to pentamidine in ATCC 17978 and mutants could be altered by bioavailability of iron or utilization of different carbon sources. In conclusion, the results of this study provide evidence that AdeAB in ATCC 17978 can confer intrinsic resistance to a subset of dicationic compounds and in particular, resistance to pentamidine can be significantly altered depending on the growth conditions.

Indexed as

Acinetobacter baumanniiAcinetobacter InfectionsAnti-Bacterial AgentsBacterial ProteinsCarbonChelating AgentsComputational BiologyDrug Resistance, Multiple, BacterialGene DeletionGene Expression Regulation, BacterialGenetic Complementation TestIronMembrane Transport ProteinsMicrobial Sensitivity TestsMutationOligonucleotide Array Sequence AnalysisAdeA protein, Acinetobacter baumanniiAdeB protein, Acinetobacter baumanniiAnti-Bacterial AgentsBacterial ProteinsCarbonChelating AgentsIronMembrane Transport ProteinsPentamidine

Identifiers

PMID29750823
PMCPMC5947904
OpenAlexW2795543026

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.