Interspecies Metabolic Complementation in Cystic Fibrosis Pathogens via Purine Exchange

Date

2021

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Abstract

Cystic fibrosis (CF) is a genetic disease frequently associated with chronic lung infections caused by a consortium of pathogens. It is common for auxotrophy (the inability to biosynthesize certain essential metabolites) to develop in clinical isolates of the dominant CF pathogen Pseudomonas aeruginosa, indicating that the CF lung environment is replete in various nutrients. Many of these nutrients are likely to come from the host tissues, but some may come from the surrounding polymicrobial community within the lungs of CF patients as well. To assess the feasibility of nutrient exchange within the polymicrobial community of the CF lung, we selected P. aeruginosa and Staphylococcus aureus, two of the most prevalent species found in the CF lung environment. By comparing the polymicrobial culture of wild-type strains relative to their purine auxotrophic counterparts, we were able to observe metabolic complementation occurring in both P. aeruginosa and S. aureus when grown with a purine-producing cross-species pair. While our data indicate that some of this complementation is likely derived from extracellular DNA freed by lysis of S. aureus by the highly competitive P. aeruginosa, the partial complementation of S. aureus purine deficiency by P. aeruginosa demonstrates that bidirectional nutrient exchange between these classic competitors is possible.

Description

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited

Keywords

Auxotrophy, Purine, Cystic Fibrosis Infection, Polymicrobial Interactions, Cross Feeding, Pseudomonas aeruginosa, Staphylococcus aureus

Citation

Al Mahmud H, Baishya J, Wakeman CA. Interspecies Metabolic Complementation in Cystic Fibrosis Pathogens via Purine Exchange. Pathogens. 2021; 10(2):146. https://doi.org/10.3390/pathogens10020146

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