Find in Library

The mold <i>Aspergillus fumigatus</i> and bacterium <i>Pseudomonas aeruginosa</i> form biofilms in the airways of individuals with cystic fibrosis. Biofilm formation by <i>A. fumigatus</i> depends on the self-produced cationic exopolysaccharide galactosaminogalactan (GAG), while <i>P. aeruginosa</i> biofilms can contain the cationic exopolysaccharide Pel. GAG and Pel are rendered cationic by deacetylation mediated by either the secreted deacetylase Agd3 (<i>A. fumigatus</i>) or the periplasmic deacetylase PelA (<i>P. aeruginosa</i>). Given the similarities between these polymers, the potential for biofilm interactions between these organisms were investigated. <i>P. aeruginosa</i> were observed to adhere to <i>A. fumigatus</i> hyphae in a GAG-dependent manner and to GAG-coated coverslips of <i>A. fumigatus</i> biofilms. In biofilm adherence assays, incubation of <i>P. aeruginosa</i> with <i>A. fumigatus</i> culture supernatants containing de-<i>N</i>-acetylated GAG augmented the formation of adherent <i>P. aeruginosa</i> biofilms, increasing protection against killing by the antibiotic colistin. Fluorescence microscopy demonstrated incorporation of GAG within <i>P. aeruginosa</i> biofilms, suggesting that GAG can serve as an alternate biofilm exopolysaccharide for this bacterium. In contrast, Pel-containing bacterial culture supernatants only augmented the formation of adherent <i>A. fumigatus</i> biofilms when antifungal inhibitory molecules were removed. This study demonstrates biofilm interaction via exopolysaccharides as a potential mechanism of co-operation between these organisms in chronic lung disease.