Candida albicans is the most important fungal pathogen that causes infections in humans. Biofilms are hard-to-treat structures due to their high antifungal resistance. Saliva is a fluid that contains antimicrobial substances acting as the first-line of defense against pathogens, and its immune components may be potential tools for the discovery of new treatments against candidiasis. To evaluate the activity of histatin 5 and human lactoferrin against biofilm formation. A fluconazole-resistant Candida albicans clinical isolate was used as the model microorganism. Morphogenesis was evaluated by differential counting. Biofilm quantification was performed by XTT reduction assay. Thickness and topography of biofilms were assessed through confocal laser scanning microscopy (CLSM). Histatin 5 inhibited yeastto-hyphae transition in a dose-dependent manner, while the effect of human lactoferrin on this process was inversely proportional to its concentration. Both compounds were able to significantly inhibit biofilm metabolic activity. Histatin 5 reduced biofilm thickness. Histatin 5 and human lactoferrin exhibited in vitro cytotoxicity against a fluconazole-resistant Candida albicans biofilm, which points to the potential application of these compounds in the treatment of biofilms formed by this fungus, especially in resistant infections.

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Candida species can cause infections that range from superficial to life-threatening events. Candida albicans is an opportunistic pathogen of human microbiota, and it is frequently described as a commensal organism, but in many cases, it can assume a pathogenic behavior. The increasing number of immunocompromised patients has promoted an increase in the incidence of microorganisms that are resistant to conventional therapy. Additionally, the limited number of antifungal drugs has made the search for new compounds extremely relevant. In this study, we determined the minimal inhibitory concentrations (MICs) of two synthetic imidazoles derived from b-lapachone, namely 3-indol carboxaldehyde and p-N(CH 3 )2-benzaldehyde against a clinical isolate of C. albicans resistant to fluconazole and the reference strain ATCC 10231. Both strains had their growth affected by 3-indol carboxaldehyde, and the MICs were calculated as 31.7 and 41 lg ml -1 for ATCC 10231 and the clinical isolate, respectively. However, the p-N(CH 3 )2-benzaldehyde MIC values were above 100 lg ml -1 for both strains. Morphogenesis assays revealed that 3-indol carboxaldehyde inhibited significantly the germ tube transformation process. Moreover, this azole was also able to interfere significantly with biofilm formation of both strains, and also demonstrated the ability to disaggregate mature biofilms. The results obtained in this study indicate that 3-indol carboxaldehyde may be considered a viable alternative in modulating C. albicans biofilm and viability.