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Methods for Detecting Cytotoxic Amyloids Following Infection of Pulmonary Endothelial Cells by Pseudomonas aeruginosa
Published on: July 12, 2018
Pseudomonas aeruginosa-catecholamine inotrope interactions: a contributory factor in the development of
Primrose P Freestone1, Robert A Hirst2, Sara M Sandrini1
1Department of Infection, Immunity and Inflammation, University of Leicester School of Medicine, Leicester, England.
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.
Insights
Catecholamine inotropes significantly boost Pseudomonas aeruginosa growth and virulence, contributing to ventilator-associated pneumonia. Vasopressin and phenylephrine did not show these effects, suggesting specific drug interactions are key.
Area of Science:
- Microbiology
- Intensive Care Medicine
- Pharmacology
Background:
- Ventilator-associated pneumonia (VAP) poses significant risks in intensive care units (ICUs).
- Pseudomonas aeruginosa is a common cause of VAP, but its prevalence in ICUs is not fully understood.
Purpose of the Study:
- To investigate the impact of catecholamine inotropes on the growth and virulence of Pseudomonas aeruginosa.
- To explore the mechanisms behind Pseudomonas aeruginosa infections in ventilated patients.
Main Methods:
- In vitro and ex vivo assays were used to assess the effects of clinically relevant inotrope concentrations on P. aeruginosa.
- Experiments involved bacterial growth, virulence assays, biofilm formation, and interaction with human respiratory epithelium.
Main Results:
- Inotropes increased P. aeruginosa growth up to 50-fold by delivering iron and upregulating pyoverdine.
- Catecholamines enhanced biofilm formation on endotracheal tubing and increased P. aeruginosa toxicity to respiratory epithelium.
- Inotropes facilitated P. aeruginosa recovery from tobramycin, while vasopressin and phenylephrine had no stimulatory effect.
Conclusions:
- Catecholamine inotrope-bacterial interactions represent a potential factor in P. aeruginosa VAP development.
- Targeting these interactions could offer new strategies for VAP prevention and treatment.
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