Trophic cooperation promotes bacterial survival of Staphylococcus aureus and Pseudomonas aeruginosa
Preprint posted on 18 June 2020 https://www.biorxiv.org/content/10.1101/2020.06.17.156968v1
Article now published in The ISME Journal at http://dx.doi.org/10.1038/s41396-020-00741-9
Co-existence of S. aureus and P. aeruginosa in cystic fibrosis infections is promoted by shared metabolic pathwaysSelected by Josie Gibson
The lung is populated by many microorganisms, including pathogenic species. Cystic fibrosis (CF) is a disease which causes production of sticky mucus, which can promote microbial infections. Pseudomonas aeruginosa and Staphylococcus aureus are the most prevalent pathogens found in CF patients and interactions between P. aeruginosa and S. aureus have been established. In some cases, defined as competitive, P. aeruginosa can target S. aureus with virulence factors. However, there are some non-competitive interactions which are associated with chronic infection in CF, defined as co-existing. P. aeruginosa adaption to the infection environment and antimicrobial treatments is thought to be responsible for the establishment of co-existing infections . The aim of this study is to compare gene expression of P. aeruginosa in co-culture with S. aureus between competitive and co-existing strains using transcriptomics.
The primary finding of this study is that co-existence of P. aeruginosa and S. aureus may be caused by trophic cooperation in chronic cystic fibrosis cases. Changes in P. aeruginosa gene expression in the presence of S. aureus were compared between competitive or co-existing pairs of each pathogen, which had been isolated together from patients. In competitive scenarios, the presence of S. aureus significantly altered the expression of 68 P. aeruginosa genes. In co-existence settings, 105 P. aeruginosa genes where significantly altered by S. aureus in co-culture, where the majority of genes identified were involved in metabolism, specifically an up-regulation of genes required for the use of alternative carbon sources, including amino acids and acetoin. These observations were confirmed with RT-qPCR using further patient samples.
The role of altered P. aeruginosa metabolism gene expression to cause the ability to co-exist with S. aureus was next examined. The authors make the important observations that S. aureus produces acetoin, and that acetoin is present in CF patients. Next, it is demonstrated that acetoin produced by S. aureus induces changes in P. aeruginosa gene expression, which subsequently promotes P. aeruginosa acetoin catabolism, useful as an alternative carbon source. Interestingly, the production of acetoin by S. aureus was higher in the co-existing strains in comparison to competitive strains. Equally, co-existing P. aeruginosa was better able to catabolise acetoin than competitive strains. The authors suggest these attributes of co-existing strains are due to adaptation in chronic CF infections. Although acetoin represents a useful alternative carbon source for P. aeruginosa, high concentrations of acetoin were shown to reduce S. aureus growth, so a positive role of acetoin for S. aureus was next examined. S. aureus had reduced survival in co-culture with P. aeruginosa strains deficient in acetoin catabolism in comparison to wild-type P. aeruginosa. This indicates that P. aeruginosa acetoin catabolism is beneficial for S. aureus too, by protecting against toxic levels of acetoin. Therefore, both S. aureus and P. aeruginosa benefit from acetoin through a shared metabolic pathway.
Why I chose this Preprint:
Understanding complex polymicrobial interactions in human infection may be important for future therapeutic developments. P. aeruginosa and S. aureus are often found together in CF cases, and although the ability of P. aeruginosa to kill S. aureus is established, in chronic CF infections P. aeruginosa and S. aureus can co-exist. This study reveals that two pathogens benefit from shared metabolic pathways, based on acetoin production and catabolism, which likely promote their ability to cause chronic infection.
Questions to the authors:
- Could acetoin be a carbon source produced by other microbiota species which may indirectly promote S. aureus co-existence with P. aeruginosa?
- The changes to P. aeruginosa gene expression of liuA (involved in leucine metabolism) requires an interaction with S. aureus, do you have a suggestion of what role liuA may play in co-existing infections?
- The production of acetoin by S. aureus was increased in the presence of the co-existing P. aeruginosa strain, perhaps suggesting that S. aureus senses and responds to P. aeruginosa, do you know how this effect is caused?
- Baldan R, Cigana C, Testa F, Bianconi I, De Simone M, Pellin D, et al. Adaptation of Pseudomonas aeruginosa in Cystic Fibrosis airways influences virulence of Staphylococcus aureus in vitro and murine models of co-infection. PLoS One. 2014;9(3):e89614.
Posted on: 26 June 2020 , updated on: 25 March 2021
doi: https://doi.org/10.1242/prelights.22293Read preprint
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