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Conference Paper: Oral commensals and pathogens enhance hBD-2 expression in HOKs

TitleOral commensals and pathogens enhance hBD-2 expression in HOKs
Authors
KeywordsHost-microbial interactions
Immune response
Immunology
Microbiology and Periodontal disease
Issue Date2013
PublisherSage Publications, Inc. The Journal's web site is located at http://www.sagepub.com/journalsProdDesc.nav?prodId=Journal201925
Citation
The 2nd Meeting of the International Association of Dental Research - Asia Pacific Region (IADR-APR), Bangkok, Thailand, 21-23 August 2013. In Journal of Dental Research, 2013, v. 92 n. Special Issue B: abstract no. 14 How to Cite?
AbstractObjectives: Human β-defensins (hBDs) are antimicrobial peptides expressed by epithelial cells and leukocytes that resist the microbial colonization. Notably, hBD-2 has both antibacterial activity and chemoattractant effects, and therefore plays a vital role in innate immune system. The present study investigated hBD-2 expression in a model of human oral keratinocytes (HOKs) in response to oral commensal and periodontopathogenic bacteria. Cell surface receptors involved in the bacteria-host interaction were examined. Methods: Representative oral commensal bacteria (Streptococcus mitis, Smi and Streptococcus sanguinis, Ss) and pathogenic bacteria (Porphyromonas gingivalis, Pg) were selected. The expression of hBD-2 in the interaction of HOKs with the species was assessed in a bacteria-HOKs co-culture model during a time course of 15 to 120 min, using both ELISA and qPCR. Toll-like receptors (TLR) 2 and 4 were analyzed using qPCR and antibody-mediated blocking assays. Results: Multiplicity of infection (MOI) 10 was found to be appropriate for the co-culture model. Overall, Smi, Ss and Pg significantly upregulated the expression of hBD-2 in HOKs with reference to the control (p<0.05). As compared to the control Ss and Pg greatly stimulated hBD-2 expression at 30 (p<0.05), 60 (p<0.01) and 120 min (p<0.05). Whereas, the significant upregulation of hBD-2 was only observed at 60 and 120 min in HOKs stimulated by Smi. Blocking assays showed that Smi- and Ss-stimulated expression of hBD-2 in HOKs was through both TLRs 2 and 4, while blockage of TLRs 2 and 4 did not significantly affect hBD-2 expression. Conclusion: This study suggests that hBD-2 expression in HOKs may be significantly enhanced by the challenge of Smi, Ss and Pg. TLRs 2 and 4 are involved in the Smi- and Ss-stimulated expression of hBD-2 in HOKs. Supported by the Hong Kong RGC (HKU768411M and HKU767512M) and the Modern Dental Laboratory/HKU Endowment Fund to LJJ.
DescriptionConference Theme: We are the Future
Oral Presentation
Session 3: O3
Persistent Identifierhttp://hdl.handle.net/10722/192566
ISSN
2015 Impact Factor: 4.602
2015 SCImago Journal Rankings: 1.714

 

DC FieldValueLanguage
dc.contributor.authorLi, Hen_US
dc.contributor.authorSeneviratne, CJen_US
dc.contributor.authorLau, ASYen_US
dc.contributor.authorWang, CYen_US
dc.contributor.authorJin, Len_US
dc.date.accessioned2013-11-18T05:06:40Z-
dc.date.available2013-11-18T05:06:40Z-
dc.date.issued2013en_US
dc.identifier.citationThe 2nd Meeting of the International Association of Dental Research - Asia Pacific Region (IADR-APR), Bangkok, Thailand, 21-23 August 2013. In Journal of Dental Research, 2013, v. 92 n. Special Issue B: abstract no. 14en_US
dc.identifier.issn0022-0345-
dc.identifier.urihttp://hdl.handle.net/10722/192566-
dc.descriptionConference Theme: We are the Future-
dc.descriptionOral Presentation-
dc.descriptionSession 3: O3-
dc.description.abstractObjectives: Human β-defensins (hBDs) are antimicrobial peptides expressed by epithelial cells and leukocytes that resist the microbial colonization. Notably, hBD-2 has both antibacterial activity and chemoattractant effects, and therefore plays a vital role in innate immune system. The present study investigated hBD-2 expression in a model of human oral keratinocytes (HOKs) in response to oral commensal and periodontopathogenic bacteria. Cell surface receptors involved in the bacteria-host interaction were examined. Methods: Representative oral commensal bacteria (Streptococcus mitis, Smi and Streptococcus sanguinis, Ss) and pathogenic bacteria (Porphyromonas gingivalis, Pg) were selected. The expression of hBD-2 in the interaction of HOKs with the species was assessed in a bacteria-HOKs co-culture model during a time course of 15 to 120 min, using both ELISA and qPCR. Toll-like receptors (TLR) 2 and 4 were analyzed using qPCR and antibody-mediated blocking assays. Results: Multiplicity of infection (MOI) 10 was found to be appropriate for the co-culture model. Overall, Smi, Ss and Pg significantly upregulated the expression of hBD-2 in HOKs with reference to the control (p<0.05). As compared to the control Ss and Pg greatly stimulated hBD-2 expression at 30 (p<0.05), 60 (p<0.01) and 120 min (p<0.05). Whereas, the significant upregulation of hBD-2 was only observed at 60 and 120 min in HOKs stimulated by Smi. Blocking assays showed that Smi- and Ss-stimulated expression of hBD-2 in HOKs was through both TLRs 2 and 4, while blockage of TLRs 2 and 4 did not significantly affect hBD-2 expression. Conclusion: This study suggests that hBD-2 expression in HOKs may be significantly enhanced by the challenge of Smi, Ss and Pg. TLRs 2 and 4 are involved in the Smi- and Ss-stimulated expression of hBD-2 in HOKs. Supported by the Hong Kong RGC (HKU768411M and HKU767512M) and the Modern Dental Laboratory/HKU Endowment Fund to LJJ.-
dc.languageengen_US
dc.publisherSage Publications, Inc. The Journal's web site is located at http://www.sagepub.com/journalsProdDesc.nav?prodId=Journal201925-
dc.relation.ispartofJournal of Dental Researchen_US
dc.rightsJournal of Dental Research. Copyright © Sage Publications, Inc.-
dc.subjectHost-microbial interactions-
dc.subjectImmune response-
dc.subjectImmunology-
dc.subjectMicrobiology and Periodontal disease-
dc.titleOral commensals and pathogens enhance hBD-2 expression in HOKsen_US
dc.typeConference_Paperen_US
dc.identifier.emailSeneviratne, CJ: jaya@hku.hken_US
dc.identifier.emailLau, ASY: asylau@hku.hken_US
dc.identifier.emailJin, L: ljjin@hkucc.hku.hken_US
dc.identifier.authoritySeneviratne, CJ=rp01372en_US
dc.identifier.authorityLau, ASY=rp00474en_US
dc.identifier.authorityJin, L=rp00028en_US
dc.identifier.hkuros226796en_US
dc.identifier.volume92en_US
dc.identifier.issueSpecial Issue B: abstract no. 14en_US
dc.publisher.placeUnited States-

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