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Conference Paper: P. gingivalis LPS modulation of LPS-binding protein expression in HOK

TitleP. gingivalis LPS modulation of LPS-binding protein expression in HOK
Authors
KeywordsImmunology
Epithelium/epithelial
Periodontal disease
LPS-binding protein
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. 95 How to Cite?
AbstractObjectives: LPS-binding protein (LBP) functions as a crucial molecule in innate immune response to bacterial challenge. Our previous study found LBP expression in human gingiva and human oral keratinocytes (HOK) as well as its association with periodontal health and disease. This study was to further investigate the effects of P. gingivalis LPS on LBP expression in HOK. Material and Methods: HOK were treated with P. gingivalis penta-acylated LPS (LPS1690) at 100ng/ml for 24h. The human Toll-like Receptor (TLR) signaling pathway PCR array which profiles the expression of 84 genes related to TLR-mediated transduction was selected to screen the pathways involved in the P. gingivalis LPS stimulated HOK. Small interfering RNA (siRNA) gene and antibody knock-down methods were employed in monitoring TLR2-dependent LBP expression profile. Results: A number of TLRs genes including TLR2, CD14 and TLR9 were detected in HOK stimulated by P. gingivalis LPS, while no TLR4 mRNA expression was observed. The relevant downstream pathways like NF-kappaB and IRF were also involved in the gene expression in P. gingivalis LPS treated HOK. siRNA data and antibody knock-down study showed that modulation of LBP expression by P. gingivalis LPS may be through TLR2. Conclusions: This study shows that LBP expression could be enhanced by P. gingivalis LPS1690 in HOK likely through a TLR2 dependent pathway. Supported by the Research Grants Council of Hong Kong (GRF HKU766909M to LJJ).
Persistent Identifierhttp://hdl.handle.net/10722/224282
ISSN
2015 Impact Factor: 4.602
2015 SCImago Journal Rankings: 1.714

 

DC FieldValueLanguage
dc.contributor.authorDing, P-
dc.contributor.authorDarveau, RP-
dc.contributor.authorWang, CY-
dc.contributor.authorJin, LJ-
dc.date.accessioned2016-03-31T03:55:56Z-
dc.date.available2016-03-31T03:55:56Z-
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. 95-
dc.identifier.issn0022-0345-
dc.identifier.urihttp://hdl.handle.net/10722/224282-
dc.description.abstractObjectives: LPS-binding protein (LBP) functions as a crucial molecule in innate immune response to bacterial challenge. Our previous study found LBP expression in human gingiva and human oral keratinocytes (HOK) as well as its association with periodontal health and disease. This study was to further investigate the effects of P. gingivalis LPS on LBP expression in HOK. Material and Methods: HOK were treated with P. gingivalis penta-acylated LPS (LPS1690) at 100ng/ml for 24h. The human Toll-like Receptor (TLR) signaling pathway PCR array which profiles the expression of 84 genes related to TLR-mediated transduction was selected to screen the pathways involved in the P. gingivalis LPS stimulated HOK. Small interfering RNA (siRNA) gene and antibody knock-down methods were employed in monitoring TLR2-dependent LBP expression profile. Results: A number of TLRs genes including TLR2, CD14 and TLR9 were detected in HOK stimulated by P. gingivalis LPS, while no TLR4 mRNA expression was observed. The relevant downstream pathways like NF-kappaB and IRF were also involved in the gene expression in P. gingivalis LPS treated HOK. siRNA data and antibody knock-down study showed that modulation of LBP expression by P. gingivalis LPS may be through TLR2. Conclusions: This study shows that LBP expression could be enhanced by P. gingivalis LPS1690 in HOK likely through a TLR2 dependent pathway. Supported by the Research Grants Council of Hong Kong (GRF HKU766909M to LJJ).-
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.subjectImmunology-
dc.subjectEpithelium/epithelial-
dc.subjectPeriodontal disease-
dc.subjectLPS-binding protein-
dc.titleP. gingivalis LPS modulation of LPS-binding protein expression in HOK-
dc.typeConference_Paper-
dc.identifier.emailDing, P: phding@163.com-
dc.identifier.emailJin, LJ: ljjin@hkusua.hku.hk-
dc.identifier.authorityJin, LJ=rp00028-
dc.identifier.hkuros181600-
dc.identifier.volume89-
dc.identifier.issueSpec Iss C-
dc.identifier.spageAbstract no. 95-
dc.identifier.epageAbstract no. 95-
dc.publisher.placeUnited States-

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