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Aspergillus fumigatus (Af)  and  Pseudomonas aeruginosa  ( Pa ) are leading fungal and bacterial pathogens, respectively, in many clinical situations. Relevant to this, their interface and co-existence has been studied. In some experiments  in vitro ,  Pa  products have been defined that are inhibitory to  Af . In some clinical situations, both can be biofilm producers, and biofilm could alter their physiology and affect their interaction. That may be most relevant to airways in cystic fibrosis (CF), where both are often prominent residents.  We have studied clinical  Pa  isolates from several sources for their effects on  Af , including testing involving their biofilms. We show that the described inhibition of  Af  is related to the source and phenotype of the  Pa  isolate.  Pa  cells inhibited the growth and formation of  Af  biofilm from conidia, with CF isolates more inhibitory than non-CF isolates, and non-mucoid CF isolates most inhibitory. Inhibition did not require live  Pa  contact, as culture filtrates were also inhibitory, and again non-mucoid>mucoid CF>non-CF. Preformed  Af  biofilm was more resistant to  Pa , and inhibition that occurred could be reproduced with filtrates. Inhibition of  Af  biofilm appears also dependent on bacterial growth conditions; filtrates from  Pa  grown as biofilm were more inhibitory than from  Pa  grown planktonically. The differences in  Pa  shown from these different sources are consistent with the extensive evolutionary  Pa  changes that have been described in association with chronic residence in CF airways, and may reflect adaptive changes to life in a polymicrobial environment.

plos one

Inhibition of Aspergillus fumigatus and Its Biofilm by Pseudomonas aeruginosa Is Dependent on the Source, Phenotype and Growth Conditions of the Bacterium