Coculture of Staphylococcus aureus with Pseudomonas aeruginosa Drives S. aureus towards Fermentative Metabolism and Reduced Viability in a Cystic Fibrosis Model.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
AuthorsFilkins, Laura M
Graber, Jyoti A
Olson, Daniel G
Dolben, Emily L
Lynd, Lee R
O'Toole, George A
MetadataShow full item record
AbstractThe airways of patients with cystic fibrosis are colonized with diverse bacterial communities that change dynamically during pediatric years and early adulthood. Staphylococcus aureus is the most prevalent pathogen during early childhood, but during late teens and early adulthood, a shift in microbial composition occurs leading to Pseudomonas aeruginosa community predominance in ∼50% of adults. We developed a robust dual-bacterial in vitro coculture system of P. aeruginosa and S. aureus on monolayers of human bronchial epithelial cells homozygous for the ΔF508 cystic fibrosis transmembrane conductance regulator (CFTR) mutation to better model the mechanisms of this interaction. We show that P. aeruginosa drives the S. aureus expression profile from that of aerobic respiration to fermentation. This shift is dependent on the production of both 2-heptyl-4-hydroxyquinoline N-oxide (HQNO) and siderophores by P. aeruginosa. Furthermore, S. aureus-produced lactate is a carbon source that P. aeruginosa preferentially consumes over medium-supplied glucose. We find that initially S. aureus and P. aeruginosa coexist; however, over extended coculture P. aeruginosa reduces S. aureus viability, also in an HQNO- and P. aeruginosa siderophore-dependent manner. Interestingly, S. aureus small-colony-variant (SCV) genetic mutant strains, which have defects in their electron transport chain, experience reduced killing by P. aeruginosa compared to their wild-type parent strains; thus, SCVs may provide a mechanism for persistence of S. aureus in the presence of P. aeruginosa. We propose that the mechanism of P. aeruginosa-mediated killing of S. aureus is multifactorial, requiring HQNO and P. aeruginosa siderophores as well as additional genetic, environmental, and nutritional factors.
CitationCoculture of Staphylococcus aureus with Pseudomonas aeruginosa Drives S. aureus towards Fermentative Metabolism and Reduced Viability in a Cystic Fibrosis Model. 2015, 197 (14):2252-64 J. Bacteriol.
JournalJournal of bacteriology
The following license files are associated with this item:
- Exogenous Alginate Protects Staphylococcus aureus from Killing by Pseudomonas aeruginosa.
- Authors: Price CE, Brown DG, Limoli DH, Phelan VV, O'Toole GA
- Issue date: 2020 Mar 26
- Pseudomonas aeruginosa Alters Staphylococcus aureus Sensitivity to Vancomycin in a Biofilm Model of Cystic Fibrosis Infection.
- Authors: Orazi G, O'Toole GA
- Issue date: 2017 Jul 18
- A Pseudomonas aeruginosa Antimicrobial Affects the Biogeography but Not Fitness of Staphylococcus aureus during Coculture.
- Authors: Barraza JP, Whiteley M
- Issue date: 2021 Mar 30
- Staphylococcus aureus sigma B-dependent emergence of small-colony variants and biofilm production following exposure to Pseudomonas aeruginosa 4-hydroxy-2-heptylquinoline-N-oxide.
- Authors: Mitchell G, Séguin DL, Asselin AE, Déziel E, Cantin AM, Frost EH, Michaud S, Malouin F
- Issue date: 2010 Jan 30
- Pseudomonas aeruginosa Alginate Overproduction Promotes Coexistence with Staphylococcus aureus in a Model of Cystic Fibrosis Respiratory Infection.
- Authors: Limoli DH, Whitfield GB, Kitao T, Ivey ML, Davis MR Jr, Grahl N, Hogan DA, Rahme LG, Howell PL, O'Toole GA, Goldberg JB
- Issue date: 2017 Mar 21