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Conference Paper: Solasodine inhibits Candida albicans adhesion at sub-MIC level

TitleSolasodine inhibits Candida albicans adhesion at sub-MIC level
Authors
Issue Date2016
PublisherSage Publications, Inc. The Journal's web site is located at http://jdr.sagepub.com/
Citation
The 94th General Session & Exhibition of the IADR, 3rd Meeting of the IADR Asia Pacific Region & 35th Annual Meeting of the IADR Korean Division, Seoul, Korea, 22-25 June 2016. In Journal of Dental Research, 2016, v. 95 Spec. Iss. B, abstract no. 492 How to Cite?
AbstractOBJECTIVES: To investigate the in vitro effects of solasodine on the adhesion of Candida albicans to buccal epithelial cells. METHODS: Buccal epithelial cells (BECs) were collected from healthy adults by gently rubbing the cheek mucosa with sterile swabs, and washed twice in phosphate-buffered saline. Equal volumes of BECs (105 cells/mL) and wild type C. albicans SC5314 (107 cells/mL) were incubated at 37oC for 1 h with gentle agitation in the absence or presence of sub-MIC level (60 μM) of solasodine, and filtered through 12 μm pore polycarbonate filters. Unattached cells were washed away, and the BECs were air-dried and Gram’s stained. Attached fungal cells were counted under light microscope in 50 BECs. qRT-PCR was used to evaluate variations in expression of adhesion-related genes in solasodine-treated fungal cells. Total RNA was extracted using SV Total RNA Isolation System and reverse transcribed with Superscript II. Gene expression was determined by Fast SYBR Green Master Mix with gene-specific primers, and reactions were run: 95oC incubation for 20 s, followed by 40 cycles of 95oC incubation for 1 s and 60oC for 20 s. EFB1 was used for reference. All experiments were performed in triplicate in three different occasions. Student’s t test was used, and a P-value of <0.05 was considered statistically significant. RESULTS: Solasodine inhibited C. albicans adhesion to BECs by ~52% (P < 0.05). qRT-PCR analysis showed that while the gene expression of BCR1 was not affected, the gene expression of ALS3, ECE1, and HWP1 was reduced. However, expression of ALS1 was promoted. CONCLUSIONS: The collective data of the present study suggest that solasodine suppresses C. albicans adhesion to the BECs via downregulation of the expression of adhesion-related genes ALS3, ECE1, and HWP1. This provides insights for further investigation of this compound with respect to its antifungal effectiveness in clinical intervention studies. THIS ABSTRACT IS BASED ON RESEARCH THAT WAS FUNDED ENTIRELY OR PARTIALLY BY AN OUTSIDE SOURCE: Health and Medical Research Fund, 11100992
DescriptionPoster Session - Microbiology/Immunology-Oral Streptococci and Candida albicans: no. 492
Persistent Identifierhttp://hdl.handle.net/10722/229728
ISSN
2015 Impact Factor: 4.602
2015 SCImago Journal Rankings: 1.714

 

DC FieldValueLanguage
dc.contributor.authorTsang, PWK-
dc.contributor.authorYang, HP-
dc.contributor.authorLam, OLT-
dc.date.accessioned2016-08-23T14:12:55Z-
dc.date.available2016-08-23T14:12:55Z-
dc.date.issued2016-
dc.identifier.citationThe 94th General Session & Exhibition of the IADR, 3rd Meeting of the IADR Asia Pacific Region & 35th Annual Meeting of the IADR Korean Division, Seoul, Korea, 22-25 June 2016. In Journal of Dental Research, 2016, v. 95 Spec. Iss. B, abstract no. 492-
dc.identifier.issn0022-0345-
dc.identifier.urihttp://hdl.handle.net/10722/229728-
dc.descriptionPoster Session - Microbiology/Immunology-Oral Streptococci and Candida albicans: no. 492-
dc.description.abstractOBJECTIVES: To investigate the in vitro effects of solasodine on the adhesion of Candida albicans to buccal epithelial cells. METHODS: Buccal epithelial cells (BECs) were collected from healthy adults by gently rubbing the cheek mucosa with sterile swabs, and washed twice in phosphate-buffered saline. Equal volumes of BECs (105 cells/mL) and wild type C. albicans SC5314 (107 cells/mL) were incubated at 37oC for 1 h with gentle agitation in the absence or presence of sub-MIC level (60 μM) of solasodine, and filtered through 12 μm pore polycarbonate filters. Unattached cells were washed away, and the BECs were air-dried and Gram’s stained. Attached fungal cells were counted under light microscope in 50 BECs. qRT-PCR was used to evaluate variations in expression of adhesion-related genes in solasodine-treated fungal cells. Total RNA was extracted using SV Total RNA Isolation System and reverse transcribed with Superscript II. Gene expression was determined by Fast SYBR Green Master Mix with gene-specific primers, and reactions were run: 95oC incubation for 20 s, followed by 40 cycles of 95oC incubation for 1 s and 60oC for 20 s. EFB1 was used for reference. All experiments were performed in triplicate in three different occasions. Student’s t test was used, and a P-value of <0.05 was considered statistically significant. RESULTS: Solasodine inhibited C. albicans adhesion to BECs by ~52% (P < 0.05). qRT-PCR analysis showed that while the gene expression of BCR1 was not affected, the gene expression of ALS3, ECE1, and HWP1 was reduced. However, expression of ALS1 was promoted. CONCLUSIONS: The collective data of the present study suggest that solasodine suppresses C. albicans adhesion to the BECs via downregulation of the expression of adhesion-related genes ALS3, ECE1, and HWP1. This provides insights for further investigation of this compound with respect to its antifungal effectiveness in clinical intervention studies. THIS ABSTRACT IS BASED ON RESEARCH THAT WAS FUNDED ENTIRELY OR PARTIALLY BY AN OUTSIDE SOURCE: Health and Medical Research Fund, 11100992-
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.titleSolasodine inhibits Candida albicans adhesion at sub-MIC level-
dc.typeConference_Paper-
dc.identifier.emailLam, OLT: ottolam@hku.hk-
dc.identifier.authorityLam, OLT=rp01567-
dc.identifier.hkuros260783-
dc.identifier.volume95-
dc.identifier.issueSpec. Iss. B-
dc.publisher.placeUnited States-

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