File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Expression of human β-defensin-3 in gingival epithelia

TitleExpression of human β-defensin-3 in gingival epithelia
Authors
KeywordsGingival epithelia
Human β-defensin-3
Immunohistochemistry
in situ hybridization
Issue Date2005
PublisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3484&site=1
Citation
Journal Of Periodontal Research, 2005, v. 40 n. 6, p. 474-481 How to Cite?
AbstractObjective: This study aimed to investigate the expression patterns of the newly discovered human β-defensin-3 (hBD-3) in human gingiva. Background: Human β-defensins (hBDs) are a group of small, broad-spectrum, cationic antimicrobial peptides. Our recent study showed that the expression levels of hBD-1 and 2 peptides were associated with periodontal conditions. Methods: A total of 49 gingival biopsies were collected, including 33 samples from 21 patients with chronic periodontitis and 16 samples from 16 periodontally healthy subjects. The expression of hBD-3 was detected by immunohistochemistry and in situ hybridization. Double staining was undertaken to identify hBD-3 peptide-positive cells, using CD-1a and cytokeratin 20 as markers for Langerhans cells and Merkel cells, respectively. Results: hBD-3 peptide was detected in 88% of the samples, which was confined to the gingival epithelia. In healthy control subjects, hBD-3 peptide was more frequently detected in the basal layer as compared to the patients (53% vs. 18%, p < 0.05). In patients, hBD-3 expression extended from the basal layer to the spinous layers (82%), in which hBD-3 was confined to the basal and deep spinous layers in clinically healthy tissues from patients, whereas it extended to the superficial spinous layers in pocket tissues from patients (0% vs. 50%, p < 0.05). In both groups, hBD-3 peptide was expressed not only in gingival keratinocytes, but also in Langerhans cells and Merkel cells. hBD-3 transcripts were detected in 90% of the samples and they were confined to the basal and/or suprabasal layers of gingival epithelia. Conclusions: This study shows that hBD-3 is frequently expressed in gingival epithelia. The appropriate expression of hBD-3 peptide may contribute to the maintenance of periodontal homeostasis, possibly through its antimicrobial effect and promotion of adaptive immune responses. © Blackwell Munksgaard 2005.
Persistent Identifierhttp://hdl.handle.net/10722/154371
ISSN
2023 Impact Factor: 3.4
2023 SCImago Journal Rankings: 0.895
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLu, Qen_US
dc.contributor.authorSamaranayake, LPen_US
dc.contributor.authorDarveau, RPen_US
dc.contributor.authorJin, Len_US
dc.date.accessioned2012-08-08T08:24:56Z-
dc.date.available2012-08-08T08:24:56Z-
dc.date.issued2005en_US
dc.identifier.citationJournal Of Periodontal Research, 2005, v. 40 n. 6, p. 474-481en_US
dc.identifier.issn0022-3484en_US
dc.identifier.urihttp://hdl.handle.net/10722/154371-
dc.description.abstractObjective: This study aimed to investigate the expression patterns of the newly discovered human β-defensin-3 (hBD-3) in human gingiva. Background: Human β-defensins (hBDs) are a group of small, broad-spectrum, cationic antimicrobial peptides. Our recent study showed that the expression levels of hBD-1 and 2 peptides were associated with periodontal conditions. Methods: A total of 49 gingival biopsies were collected, including 33 samples from 21 patients with chronic periodontitis and 16 samples from 16 periodontally healthy subjects. The expression of hBD-3 was detected by immunohistochemistry and in situ hybridization. Double staining was undertaken to identify hBD-3 peptide-positive cells, using CD-1a and cytokeratin 20 as markers for Langerhans cells and Merkel cells, respectively. Results: hBD-3 peptide was detected in 88% of the samples, which was confined to the gingival epithelia. In healthy control subjects, hBD-3 peptide was more frequently detected in the basal layer as compared to the patients (53% vs. 18%, p < 0.05). In patients, hBD-3 expression extended from the basal layer to the spinous layers (82%), in which hBD-3 was confined to the basal and deep spinous layers in clinically healthy tissues from patients, whereas it extended to the superficial spinous layers in pocket tissues from patients (0% vs. 50%, p < 0.05). In both groups, hBD-3 peptide was expressed not only in gingival keratinocytes, but also in Langerhans cells and Merkel cells. hBD-3 transcripts were detected in 90% of the samples and they were confined to the basal and/or suprabasal layers of gingival epithelia. Conclusions: This study shows that hBD-3 is frequently expressed in gingival epithelia. The appropriate expression of hBD-3 peptide may contribute to the maintenance of periodontal homeostasis, possibly through its antimicrobial effect and promotion of adaptive immune responses. © Blackwell Munksgaard 2005.en_US
dc.languageengen_US
dc.publisherWiley-Blackwell Publishing, Inc.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3484&site=1en_US
dc.relation.ispartofJournal of Periodontal Researchen_US
dc.subjectGingival epithelia-
dc.subjectHuman β-defensin-3-
dc.subjectImmunohistochemistry-
dc.subjectin situ hybridization-
dc.subject.meshAdolescenten_US
dc.subject.meshAdulten_US
dc.subject.meshAnti-Infective Agents - Analysisen_US
dc.subject.meshAntigens, Cd1 - Analysisen_US
dc.subject.meshEpithelium - Pathologyen_US
dc.subject.meshGingiva - Pathologyen_US
dc.subject.meshHumansen_US
dc.subject.meshIntermediate Filament Proteins - Analysisen_US
dc.subject.meshKeratin-20en_US
dc.subject.meshKeratinocytes - Pathologyen_US
dc.subject.meshLangerhans Cells - Pathologyen_US
dc.subject.meshMerkel Cells - Pathologyen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPeriodontal Pocket - Pathologyen_US
dc.subject.meshPeriodontitis - Pathologyen_US
dc.subject.meshBeta-Defensins - Analysisen_US
dc.titleExpression of human β-defensin-3 in gingival epitheliaen_US
dc.typeArticleen_US
dc.identifier.emailSamaranayake, LP:lakshman@hku.hken_US
dc.identifier.emailJin, L:ljjin@hkucc.hku.hken_US
dc.identifier.authoritySamaranayake, LP=rp00023en_US
dc.identifier.authorityJin, L=rp00028en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1600-0765.2005.00827.xen_US
dc.identifier.pmid16302926-
dc.identifier.scopuseid_2-s2.0-27944437531en_US
dc.identifier.hkuros112532-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-27944437531&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume40en_US
dc.identifier.issue6en_US
dc.identifier.spage474en_US
dc.identifier.epage481en_US
dc.identifier.isiWOS:000232893600008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLu, Q=36128876000en_US
dc.identifier.scopusauthoridSamaranayake, LP=7102761002en_US
dc.identifier.scopusauthoridDarveau, RP=7006419856en_US
dc.identifier.scopusauthoridJin, L=7403328850en_US
dc.identifier.citeulike371826-
dc.identifier.issnl0022-3484-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats