Pseudomonas aeruginosa and their small diffusible extracellular molecules inhibit Aspergillus fumigatus biofilm formation

Authors


  • Editor: Jan Dijksterhuis

Correspondence: Gordon Ramage, Infection and Immunity Research Group, Glasgow Dental School and Hospital, School of Medicine, College of Medicine, Veterinary and Life Sciences, Faculty of Medicine, University of Glasgow, 378 Sauchiehall Street, Glasgow G2 3JZ, UK. Tel.: +44 0 141 211 9752; fax: +44 0 141 331 2798; e-mail: g.ramage@dental.gla.ac.uk

Abstract

Aspergillus fumigatus is often isolated from the lungs of cystic fibrosis (CF) patients, but unlike in severely immunocompromised individuals, the mortality rates are low. This suggests that competition from bacteria within the CF lung may be inhibitory. The purpose of this study was to investigate how Pseudomonas aeruginosa influences A. fumigatus conidial germination and biofilm formation. Aspergillus fumigatus biofilm formation was inhibited by direct contact with P. aeruginosa, but had no effect on preformed biofilm. A secreted heat-stable soluble factor was also shown to exhibit biofilm inhibition. Coculture of P. aeruginosa quorum-sensing mutants (PAO1:ΔLasI, PAO1:ΔLasR) did not significantly inhibit A. fumigatus biofilms (52.6–58.8%) to the same extent as that of the PA01 wild type (22.9–30.1%), both by direct and by indirect interaction (P<0.001). Planktonic and sessile inhibition assays with a series of short carbon chain molecules (decanol, decanoic acid and dodecanol) demonstrated that these molecules could both inhibit and disrupt biofilms in a concentration-dependent manner. Overall, this suggests that small diffusible and heat-stable molecules may be responsible for the competitive inhibition of filamentous fungal growth in polymicrobial environments such as the CF lung.

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