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Article: Transcriptional regulation of drug-resistance genes in Candida albicans biofilms in response to antifungals

TitleTranscriptional regulation of drug-resistance genes in Candida albicans biofilms in response to antifungals
Authors
Issue Date2011
PublisherSociety for General Microbiology. The Journal's web site is located at http://jmm.sgmjournals.org
Citation
Journal Of Medical Microbiology, 2011, v. 60 n. 9, p. 1241-1247 How to Cite?
AbstractBiofilm formation is a major virulence attribute of Candida albicans and is directly associated with therapeutic failure. One method by which Candida acquires antifungal resistance is the expression of drug-resistance genes. This study aimed to evaluate the transcriptional regulation of several genes associated with antifungal resistance of C. albicans under planktonic, recently adhered and biofilm growth modes and in C. albicans biofilms in response to antifungal agents. Initially, the antifungal susceptibility of C. albicans cultures in different growth modes was evaluated by standard antifungal susceptibility testing. Next, to assess CDR1, CDR2, MDR1, ERG11, FKS1 and PIL1 expression, RNA was harvested from cells in each growth mode, and from biofilms after drug treatment, and subjected to quantitative real-time RT-PCR (qRT-PCR). Biofilm C. albicans was more resistant to antifungals than recently adhered cells and stationaryphase planktonic cultures. Transcriptional expression of CDR1, CDR2, MDR1, ERG11 and FKS1 was lower in recently adhered C. albicans than in the stationary-phase planktonic cultures. In contrast, PIL1 levels were significantly increased in recently adhered and biofilm modes of growth. The expression of MDR1 in biofilms greatly increased on challenge with amphotericin B but not with the other drugs tested (P<0.01). ERG11 was significantly upregulated by ketoconazole (P<0.01). Caspofungin and amphotericin B significantly upregulated FKS1 expression, whereas they significantly downregulated PIL1 expression (P<0.01). These results indicate that the expression of drug-resistance genes is associated with higher drug resistance of Candida biofilms, and lay a foundation for future large-scale genome-wide expression analysis. © 2011 SGM.
Persistent Identifierhttp://hdl.handle.net/10722/137185
ISSN
2023 Impact Factor: 2.4
2023 SCImago Journal Rankings: 0.752
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grants Council, RGCHKU 7624/06M
HKU200907176121
Funding Information:

This work was supported by the Hong Kong Research Grants Council, RGC no. HKU 7624/06M to L. P. S. and HKU internal funding 200907176121 to C. J. S. We thank Dr Trevor Lane for editorial assistance.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorWatamoto, Ten_HK
dc.contributor.authorSamaranayake, LPen_HK
dc.contributor.authorEgusa, Hen_HK
dc.contributor.authorYatani, Hen_HK
dc.contributor.authorSeneviratne, CJen_HK
dc.date.accessioned2011-08-26T14:18:07Z-
dc.date.available2011-08-26T14:18:07Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Medical Microbiology, 2011, v. 60 n. 9, p. 1241-1247en_HK
dc.identifier.issn0022-2615en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137185-
dc.description.abstractBiofilm formation is a major virulence attribute of Candida albicans and is directly associated with therapeutic failure. One method by which Candida acquires antifungal resistance is the expression of drug-resistance genes. This study aimed to evaluate the transcriptional regulation of several genes associated with antifungal resistance of C. albicans under planktonic, recently adhered and biofilm growth modes and in C. albicans biofilms in response to antifungal agents. Initially, the antifungal susceptibility of C. albicans cultures in different growth modes was evaluated by standard antifungal susceptibility testing. Next, to assess CDR1, CDR2, MDR1, ERG11, FKS1 and PIL1 expression, RNA was harvested from cells in each growth mode, and from biofilms after drug treatment, and subjected to quantitative real-time RT-PCR (qRT-PCR). Biofilm C. albicans was more resistant to antifungals than recently adhered cells and stationaryphase planktonic cultures. Transcriptional expression of CDR1, CDR2, MDR1, ERG11 and FKS1 was lower in recently adhered C. albicans than in the stationary-phase planktonic cultures. In contrast, PIL1 levels were significantly increased in recently adhered and biofilm modes of growth. The expression of MDR1 in biofilms greatly increased on challenge with amphotericin B but not with the other drugs tested (P<0.01). ERG11 was significantly upregulated by ketoconazole (P<0.01). Caspofungin and amphotericin B significantly upregulated FKS1 expression, whereas they significantly downregulated PIL1 expression (P<0.01). These results indicate that the expression of drug-resistance genes is associated with higher drug resistance of Candida biofilms, and lay a foundation for future large-scale genome-wide expression analysis. © 2011 SGM.en_HK
dc.languageengen_US
dc.publisherSociety for General Microbiology. The Journal's web site is located at http://jmm.sgmjournals.orgen_HK
dc.relation.ispartofJournal of Medical Microbiologyen_HK
dc.rightsJournal of Medical Microbiology. Copyright © Society for General Microbiology.en_US
dc.subject.meshAntifungal Agents - metabolism - pharmacology-
dc.subject.meshBiofilms - drug effects - growth and development-
dc.subject.meshCandida albicans - drug effects - physiology-
dc.subject.meshDrug Resistance, Fungal-
dc.subject.meshGene Expression Regulation, Fungal - drug effects-
dc.titleTranscriptional regulation of drug-resistance genes in Candida albicans biofilms in response to antifungalsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-2615&volume=60&issue=9&spage=1241&epage=1247&date=2011&atitle=Transcriptional+regulation+of+drug-resistance+genes+in+Candida+albicans+biofilms+in+response+to+antifungalsen_US
dc.identifier.emailSamaranayake, LP:lakshman@hku.hken_HK
dc.identifier.emailSeneviratne, CJ:jaya@hku.hken_HK
dc.identifier.authoritySamaranayake, LP=rp00023en_HK
dc.identifier.authoritySeneviratne, CJ=rp01372en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1099/jmm.0.030692-0en_HK
dc.identifier.pmid21474609-
dc.identifier.scopuseid_2-s2.0-80051718125en_HK
dc.identifier.hkuros191871en_US
dc.identifier.hkuros197241en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80051718125&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume60en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1241en_HK
dc.identifier.epage1247en_HK
dc.identifier.eissn1473-5644-
dc.identifier.isiWOS:000295018700003-
dc.publisher.placeUnited Kingdomen_HK
dc.relation.projectCandida biofilms: molecular mechanisms and clinical implications-
dc.identifier.scopusauthoridWatamoto, T=24171949100en_HK
dc.identifier.scopusauthoridSamaranayake, LP=7102761002en_HK
dc.identifier.scopusauthoridEgusa, H=6602170721en_HK
dc.identifier.scopusauthoridYatani, H=7004428080en_HK
dc.identifier.scopusauthoridSeneviratne, CJ=6701897753en_HK
dc.identifier.issnl0022-2615-

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