Two bacterial species known to be frequent sources of lung infection in people with cystic fibrosis (CF) — Pseudomonas aeruginosa and Staphylococcus aureus — can feed each other with a nutrient called purine that both need to thrive, a study shows.
Such interaction could determine the course of CF, a disease in which a main cause of morbidity is lung infection.
The study, “Interspecies Metabolic Complementation in Cystic Fibrosis Pathogens via Purine Exchange,” was published in the journal Pathogens and conducted by a team of researchers at Texas Tech University.
Mucus is required in the lungs to clear foreign particles. But the mucus of CF patients is excessively viscous, and patients’ airways are typically obstructed due to thick and sticky mucus. This promotes lung infections, and can lead to respiratory symptoms.
Two of the most common species causing lung infections in CF patients are P. aeruginosa and S. aureus.
“The complex interplay between these organisms plays a vital role in disease progression and pathogenesis,” the researchers wrote.
One way these bacteria can interact is via nutrient exchange. Some bacteria are unable to make a particular metabolite, or nutrient that provides nourishment essential for their growth, and they need to obtain it from the surrounding environment.
Using a series of experiments in vitro (cultures in a lab dish), the researchers found that P. aeruginosa lacking the ability to make purine — a molecule used to build other, more complex molecules that are essential for life — thrived when placed with purine-producing S. aureus, indicating that P. aeruginosa used the purine provided by S. aureus to grow.
Previous studies have shown that chronic lung infections in CF are associated with biofilms, the communities of bacteria that attach tightly to each other and to surfaces, and that these biofilms are rich in exogenous DNA (DNA originating outside the organism).
Such exogenous DNA “may be sourced from dead microbial cells or from host innate immune components,” the researchers wrote.
Researchers wondered whether the growth of purine-deficient P. aeruginosa could also be rescued by exogenous DNA that is released by S. aureus. They found that S. aureus indeed releases exogenous DNA through cell lysis (cell breakdown), but the amount was not enough to completely rescue the growth of purine-deficient P. aeruginosa.
Next, the researchers performed a similar set of experiments, but this time the bacteria swapped roles: S. aureus lacking the ability to make purine was placed with purine-producing P. aeruginosa. Again, the purine-deficient bacteria used the purine provided by the other bacterial species to grow.
Purine exchange between these bacteria could occur in either direction, the team noted.
“We were able to observe metabolic complementation occurring in both P. aeruginosa and S. aureus when grown with a purine-producing cross-species pair,” the researchers wrote. “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.”
According to the team, “this type of metabolic complementation could represent the first step in the evolution of cooperative/synergist interactions within polymicrobial communities.”
This mutually beneficial cohabitation could also be a reason some CF lung infections are so difficult to treat, and merits further study, the researchers wrote.
“Such interactions can have severe impacts during infection as polymicrobial synergy has been shown to increase antibiotic resistance and disease severity in certain cases,” they concluded. “Therefore, these types of interactions in the context of isolates from CF lungs and other chronic infections should be the focus of future studies.”
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