We reassessed the in vitro synergistic effect of fluconazole with the non-steroidal anti-inflammatory agent ibuprofen against the pathogenic yeast Candida albicans. No synergistic effect of fluconazole combined with ibuprofen was seen against fluconazole-susceptible strains, but a remarkable effect was seen against fluconazole-resistant strains (FIX index: 0.02-0.03). Furthermore, vigorous growth of the microorganism, the so-called 'Eagle effect', was observed at concentrations higher than the minimal inhibitory concentrations of ibuprofen and fluconazole. Our results suggest that the combination of ibuprofen and fluconazole should prove useful for treating infection caused by fluconazole-resistant C. albicans.
Bloodstream infection by the pathogenic fungus Candida albicans is a major health problem. Candidemia is often associated with medical devices, which can act as substrates for biofilm development. Biofilm-related infections are relatively difficult to treat because of their resistance to antimicrobial agents. It is therefore important to explore the mechanisms of biofilm formation. Dimorphism is a major contributor to biofilm formation in C. albicans. To determine whether the hypha-related proteins Pra1 (pH-regulated antigen) and Zrt1 (zinc transporter) are responsible for biofilm formation, the ability of pra1 and zrt1 deletion mutants to form biofilms was investigated. Biofilm formation by both deletion mutants was less than that of the wild-type strain. Because Pra1 and Zrt1 are also related to the zinc homeostasis system, the effects of adding zinc on biofilm formation were also examined. Biofilm formation was increased in the presence of zinc. These data suggest that Pra1 and Zrt1 regulate biofilm formation through zinc homeostasis.
A pathogenic yeast, Candida albicans, causes life‐threatening infection in immunocompromised patients. Inhibiting the production or release of phospholipase B by C. albicans should reduce direct host cell damage, and inhibit the release of eicosanoids from cells of this microorganism. Of the antitumor agents tested, doxorubicin and daunorubicin inhibited the activity of phospholipase B, and prostaglandin production by C. albicans. These two agents have the potential to inhibit the activity of C. albicans phospholipase B, although the inhibitory concentrations exceeded the clinical dose.
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