LAUSR

The multidrug-resistant pathogen Candida auris is characterized by its aggregation under certain conditions, which affects its biofilm formation, drug susceptibility, and pathogenicity. Although the innate tendency to aggregate depends on the strain, the mechanism regulating C. auris aggregation remains unclear. We found that the culture supernatant from one of the 95 Actinomyces strains isolated from a deep-sea environment (IMAs2016D-66) inhibited C. auris aggregation. The cells grown in the presence of IMAs2016D-66 exhibited reduced hydrophobicity, biofilm formation, and enhanced proteolytic activity. In addition, the efflux pump activity of the fluconazole-resistant C. auris strain LSEM 3673 was stimulated by IMAs2016D-66, whereas no significant change was observed in the fluconazole-susceptible strain LSEM 0643. As the relationship between aggregative tendency and virulence in C. auris is still unclear, IMAs2016D-66 can serve as a tool for investigating regulatory mechanisms of phenotype switching and virulence expression of C. auris. Understanding of phenotype switching may help us not only to understand the pathogenicity of C. auris, but also to design new drugs that target the molecules regulating virulence factors.