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Due to the high incidence of nosocomial  Candida albicans  infection, the first-line drugs for  C. albicans  infection have been heavily used, and the emergence of drug-resistant strains has gradually increased. Thus, a new antifungal drug or therapeutic method is needed. Chitosan, a product of chitin deacetylation, is considered to be potentially therapeutic for fungal infections because of its excellent biocompatibility, biodegradability and low toxicity. The biocidal action of chitosan against  C. albicans  shows great commercial potential, but the exact mechanisms underlying its antimicrobial activity are unclear. To reveal these mechanisms, mutant library screening was performed.  ADA2  gene, which encodes a histone acetylation coactivator in the SAGA complex, was identified. Transmission electronic microscopy images showed that the surface of chitosan-treated  ada2 Δ cells was substantially disrupted and displayed an irregular morphology. Interestingly, the cell wall of  ada2 Δ cells was significantly thinner than that of wild-type cells, with a thickness similar to that seen in the chitosan-treated wild-type strain. Although  ADA2  is required for chitosan tolerance, expression of  ADA2  and several Ada2-mediated cell wall-related genes ( ALS2, PGA45 , and  ACE2 ) and efflux transporter genes ( MDR1  and  CDR1 ) were significantly inhibited by chitosan. Furthermore,  GCN5  encoding a SAGA complex catalytic subunit was inhibited by chitosan, and  gcn5 Δ cells exhibited phenotypes comparable to those of  ada2 Δ cells in response to chitosan and other cell surface-disrupting agents. This study demonstrated that a potential antifungal mechanism of chitosan against  C. albicans  operates by inhibiting SAGA complex gene expression, which decreases the protection of the cell surface against chitosan.

frontiers in microbiology

A Potential Antifungal Effect of Chitosan Against Candida albicans Is Mediated via the Inhibition of SAGA Complex Component Expression and the Subsequent Alteration of Cell Surface Integrity