ArticleNucleic acids research2025
An antibiotic-responsive regulator orchestrates chronic-to-acute virulence switch in Pseudomonas aeruginosa.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Dual-functional quorum sensing signal synthases DspII and DspI coordinate virulence switch in Pseudomonas aeruginosa.Nature communications · 2026Article
- The Type VI secretion system in enteric pathogen colonization: molecular mechanisms, ecological dynamics, and therapeutic potential.Frontiers in microbiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Misuse and overuse of antibiotics have led to the rapid emergence of antibiotic-resistant superbugs. In addition, evidence is emerging that antibiotic exposure could impose substantial influence on bacterial virulence, but the underlying mechanisms remain poorly understood. Here, we discovered a highly conserved aminoglycoside-responsive regulator, AmgR, that inversely modulates the production of destructive toxins [pyocyanin (PYO) and protease] and the inter-bacterial competition weapon [type VI secretion system (H1-T6SS)], which are the signature virulence factors involved in acute and chronic infections, respectively, in Pseudomonas aeruginosa. We demonstrated that AmgR positively regulates PYO and protease productions by directly activating the transcription of their biosynthetic genes and negatively regulates H1-T6SS indirectly through the quorum sensing regulator PqsR. Importantly, we showed that AmgR can be induced by sub-inhibitory concentrations of aminoglycoside antibiotics to trigger the bacterial chronic-to-acute virulence switch, by promoting P.aeruginosa to withdraw from production of the chronic infection-associated virulence factor H1-T6SS to gear up for generation of acute infection related toxins PYO and protease. This study highlights the risks of improper antibiotic usage not only in elevating antibiotic resistance but also in reprogramming bacterial virulence to exacerbate disease dissemination and acute lethality, providing critical insights for the optimization of antibiotic therapies.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.