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Article: Differential modulation of human β-defensins expression in human gingival epithelia by Porphyromonas gingivalis lipopolysaccharide with tetra- And penta-acylated lipid A structures

TitleDifferential modulation of human β-defensins expression in human gingival epithelia by Porphyromonas gingivalis lipopolysaccharide with tetra- And penta-acylated lipid A structures
Authors
Issue Date2009
PublisherSage Publications Ltd.. The Journal's web site is located at http://ini.sagepub.com
Citation
Innate Immunity, 2009, v. 15 n. 6, p. 325-335 How to Cite?
Abstract
Porphyromonas gingivalis lipopolysaccharide (LPS) is a crucial virulence factor strongly involved in the development of chronic periodontitis. It displays a significant amount of lipid A structural heterogeneity, containing both tetra- (LPS 1435/1449) and penta-acylated (LPSi690) lipid A structures with opposing effects on E-selectin expression in human endothelial cells. Little is known about how these two isoforms of P. gingivalis LPS could differentially affect host innate immune responses in human gingival epithelia. The present study compares the modulatory effects of P. gingivalis LPS 1435/1449 and LPSi 690 on the expression of human β-defensins (hBDs) in the reconstituted human gingival epithelium, and examines the involvements of a panel of pattern recognition receptors in the modulatory effects concerned. It is shown that hBD-1, hBD-2 and hBD-3 mRNAs are significantly up-regulated by P. gingivalis LPS1690, but down-regulated by P. gingivalis LPS1435/1449. Toll-like receptor (TLR) 2 and CD14 mRNAs are also differentially regulated, and the modulation of hBD-2 expression may be through the co-operation of both TLR2 and TLR4. This study suggests that P. gingivalis LPS with different lipid A structures could differentially modulate host innate immune responses in human gingival epithelia, which may be a hitherto undescribed novel pathogenic mechanism of P. gingivalis in periodontal pathogenesis. © SAGE Publications 2009.
Persistent Identifierhttp://hdl.handle.net/10722/66619
ISSN
2013 Impact Factor: 2.459
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grants CouncilHKU 7518/05M
The University of Hong Kong
Funding Information:

This work was supported by grants from the Hong Kong Research Grants Council (HKU 7518/05M) and The University of Hong Kong (HKU CRCG 2007-2009) to LJJ.

References
Grants

 

Author Affiliations
  1. Prince Philip Dental Hospital
  2. University of California, Los Angeles
  3. University of Washington Seattle
DC FieldValueLanguage
dc.contributor.authorLu, Qen_HK
dc.contributor.authorDarveau, RPen_HK
dc.contributor.authorSamaranayake, LPen_HK
dc.contributor.authorWang, CYen_HK
dc.contributor.authorJin, Len_HK
dc.date.accessioned2010-09-06T05:47:54Z-
dc.date.available2010-09-06T05:47:54Z-
dc.date.issued2009en_HK
dc.identifier.citationInnate Immunity, 2009, v. 15 n. 6, p. 325-335en_HK
dc.identifier.issn1753-4259en_HK
dc.identifier.urihttp://hdl.handle.net/10722/66619-
dc.description.abstractPorphyromonas gingivalis lipopolysaccharide (LPS) is a crucial virulence factor strongly involved in the development of chronic periodontitis. It displays a significant amount of lipid A structural heterogeneity, containing both tetra- (LPS 1435/1449) and penta-acylated (LPSi690) lipid A structures with opposing effects on E-selectin expression in human endothelial cells. Little is known about how these two isoforms of P. gingivalis LPS could differentially affect host innate immune responses in human gingival epithelia. The present study compares the modulatory effects of P. gingivalis LPS 1435/1449 and LPSi 690 on the expression of human β-defensins (hBDs) in the reconstituted human gingival epithelium, and examines the involvements of a panel of pattern recognition receptors in the modulatory effects concerned. It is shown that hBD-1, hBD-2 and hBD-3 mRNAs are significantly up-regulated by P. gingivalis LPS1690, but down-regulated by P. gingivalis LPS1435/1449. Toll-like receptor (TLR) 2 and CD14 mRNAs are also differentially regulated, and the modulation of hBD-2 expression may be through the co-operation of both TLR2 and TLR4. This study suggests that P. gingivalis LPS with different lipid A structures could differentially modulate host innate immune responses in human gingival epithelia, which may be a hitherto undescribed novel pathogenic mechanism of P. gingivalis in periodontal pathogenesis. © SAGE Publications 2009.en_HK
dc.languageengen_HK
dc.publisherSage Publications Ltd.. The Journal's web site is located at http://ini.sagepub.comen_HK
dc.relation.ispartofInnate Immunityen_HK
dc.subject.meshAcylationen_HK
dc.subject.meshAntigens, CD14 - biosynthesis - geneticsen_HK
dc.subject.meshBacteroidaceae Infections - complications - immunologyen_HK
dc.subject.meshChronic Periodontitis - etiology - immunologyen_HK
dc.subject.meshEpithelium - drug effects - immunology - metabolism - pathologyen_HK
dc.subject.meshGene Expression Regulation - drug effects - immunologyen_HK
dc.subject.meshGingiva - pathologyen_HK
dc.subject.meshHost-Pathogen Interactionsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunity, Innateen_HK
dc.subject.meshLipid A - analogs & derivatives - pharmacologyen_HK
dc.subject.meshPorphyromonas gingivalis - immunology - pathogenicityen_HK
dc.subject.meshToll-Like Receptor 2 - biosynthesis - geneticsen_HK
dc.subject.meshToll-Like Receptor 4 - biosynthesis - geneticsen_HK
dc.subject.meshbeta-Defensins - biosynthesis - geneticsen_HK
dc.titleDifferential modulation of human β-defensins expression in human gingival epithelia by Porphyromonas gingivalis lipopolysaccharide with tetra- And penta-acylated lipid A structuresen_HK
dc.typeArticleen_HK
dc.identifier.emailSamaranayake, LP:lakshman@hku.hken_HK
dc.identifier.emailJin, L:ljjin@hkucc.hku.hken_HK
dc.identifier.authoritySamaranayake, LP=rp00023en_HK
dc.identifier.authorityJin, L=rp00028en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1177/1753425909104899en_HK
dc.identifier.pmid19675119en_HK
dc.identifier.scopuseid_2-s2.0-74549193899en_HK
dc.identifier.hkuros168449en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-74549193899&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume15en_HK
dc.identifier.issue6en_HK
dc.identifier.spage325en_HK
dc.identifier.epage335en_HK
dc.identifier.eissn1753-4267-
dc.identifier.isiWOS:000272623500001-
dc.publisher.placeUnited Kingdomen_HK
dc.relation.projectNovel molecular mechanisms of innate host defense - implications in periodontal health and disease-
dc.identifier.scopusauthoridLu, Q=36128876000en_HK
dc.identifier.scopusauthoridDarveau, RP=7006419856en_HK
dc.identifier.scopusauthoridSamaranayake, LP=7102761002en_HK
dc.identifier.scopusauthoridWang, CY=35276383300en_HK
dc.identifier.scopusauthoridJin, L=7403328850en_HK

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