File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Adhesion of oral C. albicans to human buccal epithelial cells following limited exposure to antifungal agents

TitleAdhesion of oral C. albicans to human buccal epithelial cells following limited exposure to antifungal agents
Authors
Issue Date1998
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JOPM
Citation
Journal Of Oral Pathology And Medicine, 1998, v. 27 n. 7, p. 325-332 How to Cite?
AbstractThe major aetiologic agent of oral candidosis is C. albicans, and adhesion to oral mucosal surfaces is considered a vital prerequisite for successful colonisation and subsequent infection by this agent. Although many antimycotics are available for the treatment of oral candidosis, the diluent effect of saliva and the cleansing action of the oral musculature often tend to reduce the availability of the agents below that of the effective therapeutic concentration. Therefore, the yeasts undergo only a limited exposure to the antifungals during therapy. Hence, the main aim of the present study was to determine the in vitro adhesion of ten isolates of oral C. albicans to buccal epithelial cells (BEC) following a short exposure to sublethal concentrations of four antifungal agents. The yeasts were exposed to sublethal concentrations of nystatin (x6 MIC), 5-fluorocytosine (x8 MIC), ketoconazole (x4 MIC) and fluconazole (x4 MIC) for a period of 1 h. Following subsequent removal of the drug, the adhesion of these isolates to BEC was assessed by a previously described adhesion assay. The mean percentage reductions of candidal adhesion to BEC following exposure to sublethal concentrations of nystatin, 5-fluorocytosine, ketoconazole and fluconazole were 72.88%, 16.52%, 40.16% and 24.36%, respectively. Ultrastructural studies revealed that short exposure to nystatin and the azoles (but not 5-fluorocytosine) resulted in aberrant cellular features. These findings indicate that subtherapeutic levels of antifungals may modulate candidal colonization of the oral mucosa and thereby suppress the invasive potential of the pathogen.
Persistent Identifierhttp://hdl.handle.net/10722/154032
ISSN
2015 Impact Factor: 1.859
2015 SCImago Journal Rankings: 0.731
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorEllepola, ANBen_US
dc.contributor.authorSamaranayake, LPen_US
dc.date.accessioned2012-08-08T08:22:54Z-
dc.date.available2012-08-08T08:22:54Z-
dc.date.issued1998en_US
dc.identifier.citationJournal Of Oral Pathology And Medicine, 1998, v. 27 n. 7, p. 325-332en_US
dc.identifier.issn0904-2512en_US
dc.identifier.urihttp://hdl.handle.net/10722/154032-
dc.description.abstractThe major aetiologic agent of oral candidosis is C. albicans, and adhesion to oral mucosal surfaces is considered a vital prerequisite for successful colonisation and subsequent infection by this agent. Although many antimycotics are available for the treatment of oral candidosis, the diluent effect of saliva and the cleansing action of the oral musculature often tend to reduce the availability of the agents below that of the effective therapeutic concentration. Therefore, the yeasts undergo only a limited exposure to the antifungals during therapy. Hence, the main aim of the present study was to determine the in vitro adhesion of ten isolates of oral C. albicans to buccal epithelial cells (BEC) following a short exposure to sublethal concentrations of four antifungal agents. The yeasts were exposed to sublethal concentrations of nystatin (x6 MIC), 5-fluorocytosine (x8 MIC), ketoconazole (x4 MIC) and fluconazole (x4 MIC) for a period of 1 h. Following subsequent removal of the drug, the adhesion of these isolates to BEC was assessed by a previously described adhesion assay. The mean percentage reductions of candidal adhesion to BEC following exposure to sublethal concentrations of nystatin, 5-fluorocytosine, ketoconazole and fluconazole were 72.88%, 16.52%, 40.16% and 24.36%, respectively. Ultrastructural studies revealed that short exposure to nystatin and the azoles (but not 5-fluorocytosine) resulted in aberrant cellular features. These findings indicate that subtherapeutic levels of antifungals may modulate candidal colonization of the oral mucosa and thereby suppress the invasive potential of the pathogen.en_US
dc.languageengen_US
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JOPMen_US
dc.relation.ispartofJournal of Oral Pathology and Medicineen_US
dc.subject.meshAntifungal Agents - Administration & Dosage - Pharmacologyen_US
dc.subject.meshCandida Albicans - Drug Effects - Physiology - Ultrastructureen_US
dc.subject.meshCell Adhesion - Drug Effectsen_US
dc.subject.meshCheeken_US
dc.subject.meshEpithelial Cells - Microbiology - Physiology - Ultrastructureen_US
dc.subject.meshFemaleen_US
dc.subject.meshFluconazole - Pharmacologyen_US
dc.subject.meshFlucytosine - Pharmacologyen_US
dc.subject.meshHumansen_US
dc.subject.meshKetoconazole - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMicroscopy, Electron, Scanningen_US
dc.subject.meshMouth Mucosa - Microbiology - Physiology - Ultrastructureen_US
dc.subject.meshNystatin - Pharmacologyen_US
dc.titleAdhesion of oral C. albicans to human buccal epithelial cells following limited exposure to antifungal agentsen_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.pmid9725570-
dc.identifier.scopuseid_2-s2.0-0032145392en_US
dc.identifier.hkuros34147-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032145392&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume27en_US
dc.identifier.issue7en_US
dc.identifier.spage325en_US
dc.identifier.epage332en_US
dc.identifier.isiWOS:000075469800007-
dc.publisher.placeDenmarken_US
dc.identifier.scopusauthoridEllepola, ANB=6604060863en_US
dc.identifier.scopusauthoridSamaranayake, LP=7102761002en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats