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Article: Non-steroidal anti-inflammatory drugs may modulate the protease activity of candida albicans

TitleNon-steroidal anti-inflammatory drugs may modulate the protease activity of candida albicans
Authors
Issue Date2010
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/micpath
Citation
Microbial Pathogenesis, 2010, v. 49 n. 6, p. 315-322 How to Cite?
AbstractThe phenotypic pressure exerted by non-steroidal anti-inflammatory drugs (NSAIDs) on autochthonous and pathogenic microbiota remains sparsely known. In this study, we investigated if some NSAIDs increment or diminish the secretion of aspartyl-proteases (Sap) by Candida albicans grown under different phenotypes and oxygen availability using a set of SAP knock-out mutants and other set for genes (EFG1 and CPH1) that codify transcription factors involved in filamentation and protease secretion. Pre-conditioned cells were grown under planktonic and biofilm phenotypes, in normoxia and anoxia, in the presence of plasma concentrations of acetylsalicylic acid, diclofenac, indomethacin, nimesulide, piroxicam, ibuprofen, and acetaminophen. For diclofenac, indomethacin, nimesulide, and piroxicam the secretion rates of Sap by SAP1-6, EFG1, and CPH1 mutants were similar or, even, inferior to parental wild-type strain. This suggests that neither Sap 1-6 isoenzymes nor Efg1/Cph1 pathways may be entirely responsible for protease release when exposed to these NSAIDs. Ibuprofen and acetaminophen enhanced Sap secretion rates in three environmental conditions (normoxic biofilm, normoxic planktonic and anoxic planktonic). In other hand, aspirin seems to reduce the Sap-related pathogenic behavior of candidal biofilms. Modulation of Sap activity may occur according to candidal phenotypic state, oxygen availability, and type of NSAID to which the cells are exposed. © 2010 Elsevier Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/154636
ISSN
2015 Impact Factor: 1.888
2015 SCImago Journal Rankings: 0.932
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCarvalho, APen_US
dc.contributor.authorGursky, LCen_US
dc.contributor.authorRosa, RTen_US
dc.contributor.authorRymovicz, AUMen_US
dc.contributor.authorCampelo, PMSen_US
dc.contributor.authorGrégio, AMTen_US
dc.contributor.authorKogaIto, CYen_US
dc.contributor.authorSamaranayake, LPen_US
dc.contributor.authorRosa, EARen_US
dc.date.accessioned2012-08-08T08:26:37Z-
dc.date.available2012-08-08T08:26:37Z-
dc.date.issued2010en_US
dc.identifier.citationMicrobial Pathogenesis, 2010, v. 49 n. 6, p. 315-322en_US
dc.identifier.issn0882-4010en_US
dc.identifier.urihttp://hdl.handle.net/10722/154636-
dc.description.abstractThe phenotypic pressure exerted by non-steroidal anti-inflammatory drugs (NSAIDs) on autochthonous and pathogenic microbiota remains sparsely known. In this study, we investigated if some NSAIDs increment or diminish the secretion of aspartyl-proteases (Sap) by Candida albicans grown under different phenotypes and oxygen availability using a set of SAP knock-out mutants and other set for genes (EFG1 and CPH1) that codify transcription factors involved in filamentation and protease secretion. Pre-conditioned cells were grown under planktonic and biofilm phenotypes, in normoxia and anoxia, in the presence of plasma concentrations of acetylsalicylic acid, diclofenac, indomethacin, nimesulide, piroxicam, ibuprofen, and acetaminophen. For diclofenac, indomethacin, nimesulide, and piroxicam the secretion rates of Sap by SAP1-6, EFG1, and CPH1 mutants were similar or, even, inferior to parental wild-type strain. This suggests that neither Sap 1-6 isoenzymes nor Efg1/Cph1 pathways may be entirely responsible for protease release when exposed to these NSAIDs. Ibuprofen and acetaminophen enhanced Sap secretion rates in three environmental conditions (normoxic biofilm, normoxic planktonic and anoxic planktonic). In other hand, aspirin seems to reduce the Sap-related pathogenic behavior of candidal biofilms. Modulation of Sap activity may occur according to candidal phenotypic state, oxygen availability, and type of NSAID to which the cells are exposed. © 2010 Elsevier Ltd.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/micpathen_US
dc.relation.ispartofMicrobial Pathogenesisen_US
dc.subject.meshAerobiosisen_US
dc.subject.meshAnaerobiosisen_US
dc.subject.meshAnti-Inflammatory Agents - Pharmacologyen_US
dc.subject.meshAspartic Acid Proteases - Secretionen_US
dc.subject.meshBiofilms - Drug Effects - Growth & Developmenten_US
dc.subject.meshCandida Albicans - Drug Effects - Enzymology - Growth & Developmenten_US
dc.subject.meshFungal Proteins - Secretionen_US
dc.subject.meshHumansen_US
dc.subject.meshProtein Transport - Drug Effectsen_US
dc.subject.meshVirulenceen_US
dc.titleNon-steroidal anti-inflammatory drugs may modulate the protease activity of candida albicansen_US
dc.typeArticleen_US
dc.identifier.emailSamaranayake, LP:lakshman@hku.hken_US
dc.identifier.authoritySamaranayake, LP=rp00023en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.micpath.2010.07.007en_US
dc.identifier.pmid20708674-
dc.identifier.scopuseid_2-s2.0-77957767618en_US
dc.identifier.hkuros183206-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77957767618&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume49en_US
dc.identifier.issue6en_US
dc.identifier.spage315en_US
dc.identifier.epage322en_US
dc.identifier.isiWOS:000283524000002-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridCarvalho, AP=26121094900en_US
dc.identifier.scopusauthoridGursky, LC=14827791100en_US
dc.identifier.scopusauthoridRosa, RT=35576111200en_US
dc.identifier.scopusauthoridRymovicz, AUM=36457254900en_US
dc.identifier.scopusauthoridCampelo, PMS=36166401700en_US
dc.identifier.scopusauthoridGrégio, AMT=23568114800en_US
dc.identifier.scopusauthoridKogaIto, CY=6603358858en_US
dc.identifier.scopusauthoridSamaranayake, LP=7102761002en_US
dc.identifier.scopusauthoridRosa, EAR=7004952748en_US
dc.identifier.citeulike7713221-

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