Evidence map›Paper›PMID 27021319›Full record

ArticleAntimicrobial agents and chemotherapy2016

Potentiation of Aminoglycoside Activity in Pseudomonas aeruginosa by Targeting the AmgRS Envelope Stress-Responsive Two-Component System.

Keith Poole, Christie Gilmour, Maya A Farha, Erin Mullen, Calvin Ho-Fung Lau, Eric D Brown

Open access · bronzeAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

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  6. Regulation, structure, and activity of theAntimicrobial agents and chemotherapy · 2025
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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

6 authors at 2 institutions in 1 country.

Keith PooleDepartment of Biomedical and Molecular Sciences, Botterell Hall, Queen's University, Kingston, Ontario, Canada poolek@queensu.ca.
Christie GilmourDepartment of Biomedical and Molecular Sciences, Botterell Hall, Queen's University, Kingston, Ontario, Canada.
Maya A FarhaM. G. DeGroote Institute for Infectious Disease Research and Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada.
Erin MullenDepartment of Biomedical and Molecular Sciences, Botterell Hall, Queen's University, Kingston, Ontario, Canada.
Calvin Ho-Fung LauDepartment of Biomedical and Molecular Sciences, Botterell Hall, Queen's University, Kingston, Ontario, Canada.
Eric D BrownM. G. DeGroote Institute for Infectious Disease Research and Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario, Canada.
Queen's University · CAMcMaster University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A screen for agents that potentiated the activity of paromomycin (PAR), a 4,5-linked aminoglycoside (AG), against wild-type Pseudomonas aeruginosa identified the RNA polymerase inhibitor rifampin (RIF). RIF potentiated additional 4,5-linked AGs, such as neomycin and ribostamycin, but not the clinically important 4,6-linked AGs amikacin and gentamicin. Potentiation was absent in a mutant lacking the AmgRS envelope stress response two-component system (TCS), which protects the organism from AG-generated membrane-damaging aberrant polypeptides and, thus, promotes AG resistance, an indication that RIF was acting via this TCS in potentiating 4,5-linked AG activity. Potentiation was also absent in a RIF-resistant RNA polymerase mutant, consistent with its potentiation of AG activity being dependent on RNA polymerase perturbation. PAR-inducible expression of the AmgRS-dependent genes htpX and yccA was reduced by RIF, suggesting that AG activation of this TCS was compromised by this agent. Still, RIF did not compromise the membrane-protective activity of AmgRS, an indication that it impacted some other function of this TCS. RIF potentiated the activities of 4,5-linked AGs against several AG-resistant clinical isolates, in two cases also potentiating the activity of the 4,6-linked AGs. These cases were, in one instance, explained by an observed AmgRS-dependent expression of the MexXY multidrug efflux system, which accommodates a range of AGs, with RIF targeting of AmgRS undermining mexXY expression and its promotion of resistance to 4,5- and 4,6-linked AGs. Given this link between AmgRS, MexXY expression, and pan-AG resistance in P. aeruginosa, RIF might be a useful adjuvant in the AG treatment of P. aeruginosa infections.

Indexed as

AmikacinAnti-Bacterial AgentsBacterial ProteinsDrug Resistance, Multiple, BacterialDrug SynergismGene Expression Regulation, BacterialGentamicinsHeat-Shock ProteinsHumansMembrane ProteinsMicrobial Sensitivity TestsParomomycinPseudomonas aeruginosaPseudomonas InfectionsRibostamycinRifampinAmikacinAnti-Bacterial AgentsBacterial ProteinsGentamicinsHeat-Shock ProteinsMembrane ProteinsMexXY protein, Pseudomonas aeruginosaParomomycinRibostamycinRifampin

Identifiers

PMID27021319
PMCPMC4879422
OpenAlexW2333934904

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.