Cited by 107Nosocomial Infections in ICUBacterial biofilms and quorum sensingAntibiotic Resistance in Bacteria

Pseudomonas aeruginosa -Catecholamine Inotrope Interactions

Freestone, Primrose P., Hirst, Robert A., Sandrini, Sara M., Sharaff, Fathima, Fry, Helen, Hyman, Stefan, O'Callaghan, Chris·2012·Chest

Abstract

Background Ventilated patients receiving intensive care are at significant risk of acquiring a ventilator-associated pneumonia that is associated with significant morbidity and mortality. Despite intensive research, it is still unclear why Pseudomonas aeruginosa, a microbe that rarely causes pneumonia outside of intensive care, is responsible for so many of these infections.Methods We investigated whether medications frequently prescribed to patients in the ICU, the catecholamine inotropes, were affecting the growth and virulence of P aeruginosa . Effects of clinically attainable concentrations of inotropes on P aeruginosa pathogenicity were explored using in vitro growth and virulence assays and an ex vivo model of infection using ciliated human respiratory epithelium.Results We found that inotropes were potent stimulators of P aeruginosa growth, producing upto 50-fold increases in bacterial numbers via a mechanism involving inotrope delivery of transferrin-ron,internalization of the inotrope, and upregulation of the key pseudomonal siderophore pyoverdine.Inotropes also markedly increased biofilm formation on endotracheal tubing and enhanced the biofilm production and toxicity of P aeruginosa in its interaction with respiratory epithelium.Importantly, catecholamine inotropes also facilitated the rapid recovery of P aeruginosa from tobramycin antibiotic challenge. We also tested out the effect of the inotropes vasopressin and phenylephrine on the growth and virulence of P aeruginosa and found that, in contrast to the catecholamines,these drugs had no stimulatory effect.Conclusions Collectively, our results suggest that catecholamine inotrope-bacterial interactions may be an unexpected contributory factor to the development of P aeruginosa -ventilator-associated pneumonia.

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Crossref · 10.1378/chest.11-2614

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42 of 42 references verified0 citation errors · 0 not checkable

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  • Catecholamines can behave as siderophores, causing release of iron from host-iron sequestering proteins, increasing iron availability for bacteria and enhancing bacterial growth.

    “Second, catecholamines can behave as siderophores, which cause the release of iron from host-iron sequestering proteins, increasing the availability of iron for bacteria, thereby enhancing bacterial growth (Freestone et al., 2012).”

    From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Freestone et al., 2012

  • In acute illness, the normally nutrient-poor alveolus is flooded with nutrient-rich oedema, oxygen and temperature gradients are established, and host stress signalling molecules selectively promote the growth of potential pathogens.

    “The normally nutrient-poor environment of the alveolus is flooded with nutrient-rich oedema,55 pockets of oxygen and heterogeneous temperature gradients are established,48,49 and the signalling molecules of the host stress response selectively promote the growth of potential pathogens.”

    From The microbiome and critical illness (2016) · cites this paper as [51]

  • Many daily therapies and interventions in intensive care increase intestinal permeability, bacterial translocation, and bacterial virulence.

    “Many daily therapies and interventions in intensive care increase intestinal permeability (eg, nonsteroidal anti-inflammatory drugs109 and parenteral feeding55,82), bacterial translocation (eg, antibiotics,65 corticosteroids,110 and opiates111), and bacterial virulence (eg, opiates19 and catecholamines22,51).”

    From The microbiome and critical illness (2016) · cites this paper as [51]

  • In vitro, the growth of P aeruginosa is increased by the presence of catecholamines.

    “In vitro, the growth of P aeruginosa is increased by the presence of catecholamines”

    From The microbiome and critical illness (2016) · cites this paper as [51]

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Authors
Freestone, P. P., Hirst, R. A., Sandrini, S. M., Sharaff, F., Fry, H., Hyman, S., & O'Callaghan, C.
Affiliations
University of Leicester (GB)
Venue
Chest
Publisher
Elsevier BV
Published
2012-11
Volume
142
Issue
5
Pages
1200-1210
ISSN
0012-3692 (ISSN-L)
OpenAlex
W2122984467
Cited by
107
References
42
Citations by year
2026: 1 · 2025: 8 · 2024: 15 · 2023: 3 · 2022: 8 · 2021: 6 · 2020: 10 · 2019: 14 · 2018: 5 · 2017: 6 · 2016: 8 · 2015: 11 · 2014: 5 · 2013: 6 · 2012: 1
FWCI
6.18
Type
journal article
Language
en
Open access
closed
Locations
  • CHEST Journal (publishedVersion)
  • PubMed (publishedVersion)
  • Leicester Research Archive (University of Leicester) (submittedVersion)
Topics
  • Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Nosocomial Infections in ICU
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bacterial biofilms and quorum sensing
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Medicine › Antibiotic Resistance in Bacteria
Keywords
Pseudomonas aeruginosa, ventilator-associated pneumonia, bacterial growth stimulation, pyoverdine, siderophores, biofilm formation, ciliated respiratory epithelium, vasopressin, phenylephrine, intensive care unit infections
MeSH terms
Analysis of Variance, Catecholamines, Humans, Microbial Sensitivity Tests, Pseudomonas aeruginosa, Pseudomonas Infections, Risk Factors, Virulence, Biofilms, Pneumonia, Ventilator-Associated

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