Pseudomonas aeruginosa secreted factors impair biofilm development in Candida albicansLucy J. Holcombe1,, Gordon McAlester1,, Carol A. Munro3, Brice Enjalbert3, Alistair J. P. Brown3, Neil A. R. Gow3, Chen Ding4, Geraldine Butler4, Fergal O'Gara1,2 and John P. Morrissey1
1 Department of Microbiology, University College Cork, Cork, Ireland
2 BIOMERIT Research Centre, University College Cork, Cork, Ireland
3 Institute of Medical Sciences, University of Aberdeen, Aberdeen, UK
4 School of Biomolecular and Biomedical Science, Conway Institute, University College Dublin, Dublin 4, Ireland
Signal-mediated interactions between the human opportunistic pathogens Pseudomonas aeruginosa and Candida albicans affect virulence traits in both organisms. Phenotypic studies revealed that bacterial supernatant from four P. aeruginosa strains strongly reduced the ability of C. albicans to form biofilms on silicone. This was largely a consequence of inhibition of biofilm maturation, a phenomenon also observed with supernatant prepared from non-clinical bacterial species. The effects of supernatant on biofilm formation were not mediated via interference with the yeast–hyphal morphological switch and occurred regardless of the level of homoserine lactone (HSL) produced, indicating that the effect is HSL-independent. A transcriptome analysis to dissect the effects of the P. aeruginosa supernatants on gene expression in the early stages of C. albicans biofilm formation identified 238 genes that exhibited reproducible changes in expression in response to all four supernatants. In particular, there was a strong increase in the expression of genes related to drug or toxin efflux and a decrease in expression of genes associated with adhesion and biofilm formation. Furthermore, expression of YWP1, which encodes a protein known to inhibit biofilm formation, was significantly increased. Biofilm formation is a key aspect of C. albicans infections, therefore the capacity of P. aeruginosa to antagonize this has clear biomedical implications.