Editor: Jan Dijksterhuis
Pseudomonas aeruginosa and their small diffusible extracellular molecules inhibit Aspergillus fumigatus biofilm formation
Article first published online: 22 OCT 2010
© 2010 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved
FEMS Microbiology Letters
Volume 313, Issue 2, pages 96–102, December 2010
How to Cite
Mowat, E., Rajendran, R., Williams, C., McCulloch, E., Jones, B., Lang, S. and Ramage, G. (2010), Pseudomonas aeruginosa and their small diffusible extracellular molecules inhibit Aspergillus fumigatus biofilm formation. FEMS Microbiology Letters, 313: 96–102. doi: 10.1111/j.1574-6968.2010.02130.x
- Issue published online: 18 NOV 2010
- Article first published online: 22 OCT 2010
- Accepted manuscript online: 30 SEP 2010 03:10AM EST
- Received 5 July 2010; revised 22 September 2010; accepted 23 September 2010.Final version published online 22 October 2010.
- Pseudomonas aeruginosa;
- Aspergillus fumigatus;
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.