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Conference Paper: Innate immune signaling molecules regulate the Candida and epithelial cross-talk

TitleInnate immune signaling molecules regulate the Candida and epithelial cross-talk
Authors
KeywordsGene expression
Oral biology
Cell culture
Cytokine
Issue Date2010
PublisherSage Publications, Inc. The Journal's web site is located at http://jdr.sagepub.com/
Citation
The 24th IADR-SEA Division Annual Scientific Meeting, Taipei, Taiwan, 19-21 September 2010. In Journal of Dental Research, 2010, v. 89 n. Spec Iss C, p. Abstract no. 128 How to Cite?
AbstractObjective: Cross-talk between host epithelial cells and Candida results in either passive coexistence as a commensal or transformation of the fungi into a pathogenic form. Therefore, objective of the present study was to investigate the innate immune signaling molecules that regulate the cross-talk between Candida and epithelial cells. Methods: Primary human oral keratinocytes and well characterized C. albicans wild type SC5314 (WT) and its hyphal mutants MAPK (D cph1/cph), PKA (Defg1/efg1), MAPK/PKA (DDefg1/efg1 cph1/cph1) and SAP mutants (Dsap1-3 and Dsap4-6) were used. Interaction of Candida and epithelial keratinocytes was studied in a dose- and time-dependent experiments. Cellular viability was determined by fluorescent staining using confocal microscopy. Expression of toll-like receptors, signal transduction pathway molecules, cytokines, chemokines and antimicrobial peptides was evaluated by Q-PCR and ELISA. Results: C. albicans WT and D cph1/cph, D sap1-3 and D sap4-6 infected oral epithelial cells in dose- and time- dependent manner, whilst hyphal mutants D efg1/efg1 and DD efg1/efg1 cph1/cph1 were unable to infect the epithelial cells. Compared to the control, WT and MAPK mutant significantly upregulated the expression of IL-1alpha, IL-6 and IL-8, whereas PKA pathway mutants showed lack of expression. Expression of antimicrobial peptides hBDs and RNAse 7 were inhibited by WT and MAPK mutants, but not the PKA mutant. IL-1alpha, IL-6, IL-8, TNF-alpha were increased in a time-dependent manner. Conclusion: Innate immune response of oral epithelial cells governs pathogenic transformation of commensal Candida in PKA pathway dependent mechanism (HKU grants No200807176142 for LQ and RGCNoHKU 7624/06M to LP).
Persistent Identifierhttp://hdl.handle.net/10722/224327
ISSN
2015 Impact Factor: 4.602
2015 SCImago Journal Rankings: 1.714

 

DC FieldValueLanguage
dc.contributor.authorSeneviratne, CJ-
dc.contributor.authorLu, Q-
dc.contributor.authorWong, SSW-
dc.contributor.authorLuo, W-
dc.contributor.authorSamaranayake, LP-
dc.contributor.authorJin, LJ-
dc.date.accessioned2016-03-31T09:08:45Z-
dc.date.available2016-03-31T09:08:45Z-
dc.date.issued2010-
dc.identifier.citationThe 24th IADR-SEA Division Annual Scientific Meeting, Taipei, Taiwan, 19-21 September 2010. In Journal of Dental Research, 2010, v. 89 n. Spec Iss C, p. Abstract no. 128-
dc.identifier.issn0022-0345-
dc.identifier.urihttp://hdl.handle.net/10722/224327-
dc.description.abstractObjective: Cross-talk between host epithelial cells and Candida results in either passive coexistence as a commensal or transformation of the fungi into a pathogenic form. Therefore, objective of the present study was to investigate the innate immune signaling molecules that regulate the cross-talk between Candida and epithelial cells. Methods: Primary human oral keratinocytes and well characterized C. albicans wild type SC5314 (WT) and its hyphal mutants MAPK (D cph1/cph), PKA (Defg1/efg1), MAPK/PKA (DDefg1/efg1 cph1/cph1) and SAP mutants (Dsap1-3 and Dsap4-6) were used. Interaction of Candida and epithelial keratinocytes was studied in a dose- and time-dependent experiments. Cellular viability was determined by fluorescent staining using confocal microscopy. Expression of toll-like receptors, signal transduction pathway molecules, cytokines, chemokines and antimicrobial peptides was evaluated by Q-PCR and ELISA. Results: C. albicans WT and D cph1/cph, D sap1-3 and D sap4-6 infected oral epithelial cells in dose- and time- dependent manner, whilst hyphal mutants D efg1/efg1 and DD efg1/efg1 cph1/cph1 were unable to infect the epithelial cells. Compared to the control, WT and MAPK mutant significantly upregulated the expression of IL-1alpha, IL-6 and IL-8, whereas PKA pathway mutants showed lack of expression. Expression of antimicrobial peptides hBDs and RNAse 7 were inhibited by WT and MAPK mutants, but not the PKA mutant. IL-1alpha, IL-6, IL-8, TNF-alpha were increased in a time-dependent manner. Conclusion: Innate immune response of oral epithelial cells governs pathogenic transformation of commensal Candida in PKA pathway dependent mechanism (HKU grants No200807176142 for LQ and RGCNoHKU 7624/06M to LP).-
dc.languageeng-
dc.publisherSage Publications, Inc. The Journal's web site is located at http://jdr.sagepub.com/-
dc.relation.ispartofJournal of Dental Research-
dc.rightsJournal of Dental Research. Copyright © Sage Publications, Inc.-
dc.subjectGene expression-
dc.subjectOral biology-
dc.subjectCell culture-
dc.subjectCytokine-
dc.titleInnate immune signaling molecules regulate the Candida and epithelial cross-talk-
dc.typeConference_Paper-
dc.identifier.emailSeneviratne, CJ: jaya@hku.hk-
dc.identifier.emailLu, Q: luqian123@hotmail.com-
dc.identifier.emailWong, SSW: h0616549@hku.hk-
dc.identifier.emailLuo, W: uleelaw@yahoo.com.hk-
dc.identifier.emailSamaranayake, LP: lakshman@hku.hk-
dc.identifier.emailJin, LJ: ljjin@hkusua.hku.hk-
dc.identifier.authoritySeneviratne, CJ=rp01372-
dc.identifier.authoritySamaranayake, LP=rp00023-
dc.identifier.authorityJin, LJ=rp00028-
dc.identifier.hkuros181607-
dc.identifier.volume89-
dc.identifier.issueSpec Iss C-
dc.identifier.spageAbstract no. 128-
dc.identifier.epageAbstract no. 128-
dc.publisher.placeUnited States-

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