Abstract
Candida species cause cutaneous and systemic infections with a high mortality rate, especially in immunocompromised patients. The emergence of resistance to the most common antifungal drugs, also due to biofilm formation, requires the development of alternative antifungal agents. The antimicrobial peptide VLL-28, isolated from an archaeal transcription factor, shows comparable antifungal activity against 10 clinical isolates of Candida spp. Using a fluoresceinated derivative of this peptide, we found that VLL-28 binds to the surface of planktonic cells. This observation suggested that it could exert its antifungal activity by damaging the cell wall. In addition, analyses performed on biofilms via confocal microscopy revealed that VLL-28 is differentially active on all the strains tested, with C. albicans and C. parapsilosis being the most sensitive ones. Notably, VLL-28 is the first example of an archaeal antimicrobial peptide that is active towards Candida spp. Thus, this points to archaeal microorganisms as a possible reservoir of novel antifungal agents.
Highlights
Candida species are the most prevalent opportunistic fungal pathogens worldwide
The activity of VLL-28 was investigated in terms of minimum fungicidal concentration (MFC)
The values were two-fold higher than the minimum inhibitory concentration (MIC) values for all Candida species, except C. albicans 80 and C. tropicalis isolates for which the MFC values were four-fold higher than the corresponding MICs (Table 1)
Summary
Candida species are the most prevalent opportunistic fungal pathogens worldwide. Candida spp. commonly dwell as commensal microbes colonizing the skin, oral cavities, and gastrointestinal and genital-urinary tracts of most healthy humans. Candida bloodstream infection is often associated with the presence of implanted medical devices, such as shunts, stents, prostheses, endotracheal tubes, and various types of catheters[6,7,8], on which Candida species grow as a resilient biofilm capable of withstanding high antifungal concentrations. In addition to the presence of a secreted extracellular matrix, the enhanced drug resistance shown by biofilm-embedded cells is related to (i) the local increase in cell density, (ii) the upregulation of efflux pumps, (iii) the alteration of sterols in their membranes, and iv) the www.nature.com/scientificreports/. MIC μg/mL MFC μg/mL activation of stress response mechanisms This leads to the onset of persistent cells, which are a subset of metabolically dormant yeasts cells within biofilms[20,21,22,23]
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