Structural and Functional Alterations Caused by Aureobasidin A in Clinical Resistant Strains of Candida spp

Candida species are one of the most concerning causative agents of fungal infections in humans. The treatment of invasive Candida infections is based on the use of fluconazole, but the emergence of resistant isolates has been an increasing concern which has led to the study of alternative drugs with...

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Published inJournal of fungi (Basel) Vol. 9; no. 11; p. 1115
Main Authors Rollin-Pinheiro, Rodrigo, de Moraes, Daniel, Bayona-Pacheco, Brayan, Curvelo, Jose, dos Santos-Freitas, Giulia, Xisto, Mariana, Borba-Santos, Luana, Rozental, Sonia, Ferreira-Pereira, Antonio, Barreto-Bergter, Eliana
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 01.11.2023
Subjects
Amphotericin B
Antifungal activity
Antifungal agents
aureobasidin A
Biofilms
Biosynthesis
Candida
Enzymes
Fluconazole
fungal infection
Fungal infections
Fungi
Lipids
membrane
Membrane potential
Metabolism
Oxidative stress
Sodium lauryl sulfate
Sphingolipids
Structure-function relationships
Virulence
St Louis Missouri
United States > US
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Summary:Candida species are one of the most concerning causative agents of fungal infections in humans. The treatment of invasive Candida infections is based on the use of fluconazole, but the emergence of resistant isolates has been an increasing concern which has led to the study of alternative drugs with antifungal activity. Sphingolipids have been considered a promising target due to their roles in fungal growth and virulence. Inhibitors of the sphingolipid biosynthetic pathway have been described to display antifungal properties, such as myriocin and aureobasidin A, which are active against resistant Candida isolates. In the present study, aureobasidin A did not display antibiofilm activity nor synergism with amphotericin B, but its combination with fluconazole was effective against Candida biofilms and protected the host in an in vivo infection model. Alterations in treated cells revealed increased oxidative stress, reduced mitochondrial membrane potential and chitin content, as well as altered morphology, enhanced DNA leakage and a greater susceptibility to sodium dodecyl sulphate (SDS). In addition, it seems to inhibit the efflux pump CaCdr2p. All these data contribute to elucidating the role of aureobasidin A on fungal cells, especially evidencing its promising use in clinical resistant isolates of Candida species.
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ISSN:2309-608X
2309-608X
DOI:10.3390/jof9111115