The mold and bacterium form biofilms in the airways of individuals with cystic fibrosis. Biofilm formation by depends on the self-produced cationic exopolysaccharide galactosaminogalactan (GAG), while biofilms can contain the cationic exopolysaccharide Pel. GAG and Pel are rendered cationic by deacetylation mediated by either the secreted deacetylase Agd3 () or the periplasmic deacetylase PelA (). Given the similarities between these polymers, the potential for biofilm interactions between these organisms were investigated. were observed to adhere to hyphae in a GAG-dependent manner and to GAG-coated coverslips of biofilms. In biofilm adherence assays, incubation of with culture supernatants containing de--acetylated GAG augmented the formation of adherent biofilms, increasing protection against killing by the antibiotic colistin. Fluorescence microscopy demonstrated incorporation of GAG within 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 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.