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Recent studies have shown that the transcriptional landscape of the pleiomorphic fungus Candida albicans is highly dependent upon growth conditions. Here using a dual RNA-seq approach we identified 299 C. albicans and 72 Streptococcus gordonii genes that were either upregulated or downregulated specifically as a result of co-culturing these human oral cavity microorganisms. Seventy-five C. albicans genes involved in responses to chemical stimuli, regulation, homeostasis, protein modification and cell cycle were significantly (P ≤ 0.05) upregulated, whereas 36 genes mainly involved in transport and translation were downregulated. Upregulation of filamentation-associated TEC1 and FGR42 genes, and of ALS1 adhesin gene, concurred with previous evidence that the C. albicans yeast to hypha transition is promoted by S. gordonii. Increased expression of genes required for arginine biosynthesis in C. albicans was potentially indicative of a novel oxidative stress response. The transcriptional response of S. gordonii to C. albicans was less dramatic, with only eight S. gordonii genes significantly (P ≤ 0.05) upregulated at least two-fold (glpK, rplO, celB, rplN, rplB, rpsE, ciaR and gat). The expression patterns suggest that signals from S. gordonii cause a positive filamentation response in C. albicans, whereas S. gordonii appears to be transcriptionally less influenced by C. albicans. [ABSTRACT FROM AUTHOR]

Objectives We aimed to define the phenotypic and genotypic adaptations that occur in the Burkholderia cepacia complex (BCC) during chronic infection of the cystic fibrosis (CF) lung. Methods We studied a total of 57 BCC isolates from 15 CF patients (2–6 isolates per patient), spanning infection periods ranging from 3 to 14 years. We assessed virulence using the Galleria mellonella model, and phenotypically characterized all isolates to determine how individual traits evolve during infection. Genome sequencing of selected early and late isolates provided insight into the genetic basis of the adaptations, whilst selected isolates were also studied in a murine infection model and in vitro macrophage model. Results Strikingly, during infection of 4 BCC-infected patients, the virulence of longitudinal isolates increased. Those patients were infected with either the B. cenocepacia ET-12 lineage (n = 3) or a B. multivorans outbreak strain (n = 1), both of which are linked with poor clinical outcome. Increasing virulence was uniformly correlated with increased haemolytic activity and decreased biofilm formation, consistent with the emergence of an ‘acute phenotype’. Late isolates displaying heightened virulence also exhibited altered host–pathogen interactions, with delayed clearance from Galleria and/or murine infection models, and reduced uptake by macrophages in vitro. Genome sequencing of isolates revealed evidence of convergent evolution, with comparable phenotypic adaptations arising through distinct genetic mutations. Conclusion BCC adaptation strategies within the CF lung differ from those observed in Pseudomonas aeruginosa , and may contribute to poor clinical outcome. [ABSTRACT FROM AUTHOR]