ArticlePLoS pathogens2023
A compensatory RNase E variation increases Iron Piracy and Virulence in multidrug-resistant Pseudomonas aeruginosa during Macrophage infection.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Ferroptosis: significance to zoonotic diseases and therapeutic prospects.Emerging microbes & infections · 2026Review
- Inflammasome Dynamics in the High-Risk Clone ST235 with Altered Pyoverdine Structures.International journal of molecular sciences · 2026Article
- RsmW is an iron-responsive 3' UTR derived small regulatory RNA that contributes to biofilm formation and virulence ofbioRxiv : the preprint server for biology · 2026Article
- Ferroptosis and iron-based therapies inVirulence · 2025Review
- A chronicInfection and immunity · 2025Article
- Article
- Critical functions and key interactions mediated by the RNase E scaffolding domain in Pseudomonas aeruginosa.PLoS genetics · 2025Article
- The molecular and metabolic landscape of ferroptosis in respiratory diseases: Pharmacological aspects.Journal of pharmaceutical analysis · 2025Review
- Siderophores promote cooperative interspecies and intraspecies cross-protection against antibiotics in vitro.Nature microbiology · 2024Article
- A deep insight into ferroptosis in lung disease: facts and perspectives.Frontiers in oncology · 2024Review
- The mechanism of ferroptosis and its related diseases.Molecular biomedicine · 2023Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
During chronic cystic fibrosis (CF) infections, evolved Pseudomonas aeruginosa antibiotic resistance is linked to increased pulmonary exacerbations, decreased lung function, and hospitalizations. However, the virulence mechanisms underlying worse outcomes caused by antibiotic resistant infections are poorly understood. Here, we investigated evolved aztreonam resistant P. aeruginosa virulence mechanisms. Using a macrophage infection model combined with genomic and transcriptomic analyses, we show that a compensatory mutation in the rne gene, encoding RNase E, increased pyoverdine and pyochelin siderophore gene expression, causing macrophage ferroptosis and lysis. We show that iron-bound pyochelin was sufficient to cause macrophage ferroptosis and lysis, however, apo-pyochelin, iron-bound pyoverdine, or apo-pyoverdine were insufficient to kill macrophages. Macrophage killing could be eliminated by treatment with the iron mimetic gallium. RNase E variants were abundant in clinical isolates, and CF sputum gene expression data show that clinical isolates phenocopied RNase E variant functions during macrophage infection. Together these data show how P. aeruginosa RNase E variants can cause host damage via increased siderophore production and host cell ferroptosis but may also be targets for gallium precision therapy.
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