Abstract
Pseudomonas aeruginosa and Aspergillus fumigatus frequently coexist in the airways of immunocompromised patients or individuals with cystic fibrosis. Ciprofloxacin (CIP) is a synthetic quinolone antibiotic commonly used to treat bacterial infections, such as those produced by Pseudomonas aeruginosa. CIP binds iron, and it is unclear what effect this complex would have on the mycobiome. The effects of CIP on Aspergillus were dependent on the iron levels present, and on the presence of Aspergillus siderophores. We found that CIP alone stimulated wildtype planktonic growth, but not biofilm metabolism. At high concentrations, CIP antagonized a profungal effect of iron on wildtype Aspergillus metabolism, presumably owing to iron chelation. CIP interfered with the metabolism and growth of an Aspergillus siderophore mutant, with the effect on metabolism being antagonized by iron. CIP acted synergistically with iron on the growth of the mutant, and, to a lesser extent, the wildtype. In summary, CIP can increase fungal growth or affect fungal metabolism, depending on the local iron concentration and available siderophores. Therefore, high local CIP concentrations during treatment of Pseudomonas–Aspergillus co-infections may increase the fungal burden.
Highlights
A. fumigatus and P. aeruginosa share the same polymicrobial niches, e.g., in the lungs of immunocompromised patients and people with cystic fibrosis (CF), aggravating infections [1–4]
The natural fluoroquinolone PQS has been shown to interfere with the metabolism and growth of A. fumigatus under iron-limiting conditions [8,10]
The profungal effects of CIP on the wildtype fungus were only detected at concentrations >125 μg/mL, and for planktonic growth, but not for biofilm metabolism
Summary
A. fumigatus and P. aeruginosa share the same polymicrobial niches, e.g., in the lungs of immunocompromised patients and people with cystic fibrosis (CF), aggravating infections [1–4]. Interactions of A. fumigatus and P. aeruginosa have been the topic of extensive research [5–10]. Limited studies have focused on how drugs prescribed for one of these pathogens can affect the other pathogens present in the same microenvironment. Both A. fumigatus and P. aeruginosa require and compete for iron for their growth, metabolism, and virulence, and produce siderophores for its uptake [10–12]. The iron content in the microenvironment plays an important role in A. fumigatus and P. aeruginosa interactions, and in their response to antibiotics and antifungals [14]
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