ArticleAntimicrobial agents and chemotherapy2002
In vitro low-level resistance to azoles in Candida albicans is associated with changes in membrane lipid fluidity and asymmetry.
Article in Antimicrobial agents and chemotherapy, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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54 citing papers in PubMed, 137 citations in OpenAlex.
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- Sphingolipid diversity in Candida auris: unraveling interclade and drug resistance fingerprints.FEMS yeast research · 2024Article
- Comparative Analysis of TwoCells · 2023Article
- Synergistic potential of teriflunomide with fluconazole against resistantFrontiers in cellular and infection microbiology · 2023Article
- Fluconazole resistantCell surface (Amsterdam, Netherlands) · 2022Article
- Unique roles of aminophospholipid translocase Drs2p in governing efflux pump activity, ergosterol level, virulence traits, and host-pathogen interaction in Candida albicans.International microbiology : the official journal of the Spanish Society for Microbiology · 2022Article
- Artemisinin Targets Transcription Factor PDR1 and ImpairsAntioxidants (Basel, Switzerland) · 2022Article
- The Role of Ergosterol and Sphingolipids in the Localization and Activity ofInternational journal of molecular sciences · 2022Article
- Inositol Phosphoryl Transferase, Ipt1, Is a Critical Determinant of Azole Resistance and Virulence Phenotypes inJournal of fungi (Basel, Switzerland) · 2022Article
- Elucidating the Eradication Mechanism of Perillyl Alcohol againstACS bio & med chem Au · 2022Article
- Quantitative proteomics analysis of Mycoplasma pneumoniae identifies potential macrolide resistance determinants.AMB Express · 2021Article
- Mechanistic Insight Into the Antifungal Effects of a Fatty Acid Derivative Against Drug-Resistant Fungal Infections.Frontiers in microbiology · 2020Article
- Recreation of in-host acquired single nucleotide polymorphisms by CRISPR-Cas9 reveals an uncharacterised gene playing a role in Aspergillus fumigatus azole resistance via a non-cyp51A mediated resistance mechanism.Fungal genetics and biology : FG & B · 2019Article
- The Synergism of the Small Molecule ENOblock and Fluconazole Against Fluconazole-ResistantFrontiers in microbiology · 2019Article
- Azole resistance in aThe Journal of biological chemistry · 2018Article
- Antifungal activity of osthol in vitro and enhancement in vivo through Eudragit S100 nanocarriers.Virulence · 2018Article
- Analysis of sphingolipids, sterols, and phospholipids in human pathogenicJournal of lipid research · 2017Article
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5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The present study tracks the development of low-level azole resistance in in vitro fluconazole-adapted strains of Candida albicans, which were obtained by serially passaging a fluconazole-susceptible dose-dependent strain, YO1-16 (fluconazole MIC, 16 microg ml(-1)) in increasing concentrations of fluconazole, resulting in strains YO1-32 (fluconazole MIC, 32 microg ml(-1)) and YO1-64 (MIC, 64 microg ml(-1)). We show that acquired resistance to fluconazole in this series of isolates is not a random process but is a gradually evolved complex phenomenon that involves multiple changes, which included the overexpression of ABC transporter genes, e.g., CDR1 and CDR2, and the azole target enzyme, ERG11. The sequential rise in fluconazole MICs in these isolates was also accompanied by cross-resistance to other azoles and terbinafine. Interestingly, fluorescent polarization measurements performed by using the fluorescent probe 1,6-diphenyl-1,3,5-hexatriene revealed that there was a gradual increase in membrane fluidity of adapted strains. The increase in fluidity was reflected by observed change in membrane order, which was considerably decreased (decrease in fluorescence polarization values, P value) in the adapted strain (P value of 0.1 in YO1-64, compared to 0.19 in the YO1-16 strain). The phospholipid composition of the adapted strain was not significantly altered; however, ergosterol content was reduced in YO1-64 from that in the YO1-16 strain. The asymmetrical distribution of phosphatidylethanolamine (PE) between two monolayers of plasma membrane was also changed, with PE becoming more exposed to the outer monolayer in the YO1-64 strain. The results of the present study suggest for the first time that changes in the status of membrane lipid phase and asymmetry could contribute to azole resistance in C. albicans.
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