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Article: In situ detection of apoptosis at sites of chronic bacterially induced inflammation in human gingiva

TitleIn situ detection of apoptosis at sites of chronic bacterially induced inflammation in human gingiva
Authors
Issue Date1998
Citation
Infection And Immunity, 1998, v. 66 n. 11, p. 5190-5195 How to Cite?
AbstractApoptosis is a key phenomenon in the regulation of the life span of terminally differentiated leukocytes. Human gingiva represents an established model to study immune responses to bacterial infection. In this investigation, we used the TUNEL (terminal deoxynucleotidyltransferase- mediated dUTP-biotin nick end labeling) technique to evaluate presence and topographic location of apoptosis-associated DNA damage in human gingival biopsies along with the expression of the p53 and Bcl-2 apoptosis-regulating proteins. Qualitative data analysis showed high densities of cells expressing DNA damage and p53 both within the epithelial attachment to the tooth and in the perivascular infiltrate (infiltrated connective tissue [ICT]) immediately underlying the site of chronic bacterial aggression. Topographic consistency between DNA damage- and p53-positive cells was consistently observed. Quantitative analysis of the ICT showed mean densities of DNA damage- and p53-positive cells of 345 ± 278 and 403 ± 182 cells/mm2, respectively. Numerical consistency was confirmed by multivariate regression analysis: densities of DNA damage-positive cells were significantly predicted by densities of p53-positive cells (P = 0.001, r2 = 0.84). In the ICT, cells displaying biotinylated DNA nicks were 3.8% ± 2.7% of total cellularity, while p53- and Bcl-2-positive cells represented 4.4% ± 1.7% and 15.4% ± 6.7% of total cells, respectively. It is suggested that p53 expression associated with DNA damage is a prevalent phenomenon in chronically inflamed human gingiva, and that apoptosis may be a relevant process for the maintenance of local immune homeostasis at sites of chronic bacterial challenge in vivo.
Persistent Identifierhttp://hdl.handle.net/10722/154051
ISSN
2015 Impact Factor: 3.603
2015 SCImago Journal Rankings: 2.342
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTonetti, MSen_US
dc.contributor.authorCortellini, Den_US
dc.contributor.authorLang, NPen_US
dc.date.accessioned2012-08-08T08:23:00Z-
dc.date.available2012-08-08T08:23:00Z-
dc.date.issued1998en_US
dc.identifier.citationInfection And Immunity, 1998, v. 66 n. 11, p. 5190-5195en_US
dc.identifier.issn0019-9567en_US
dc.identifier.urihttp://hdl.handle.net/10722/154051-
dc.description.abstractApoptosis is a key phenomenon in the regulation of the life span of terminally differentiated leukocytes. Human gingiva represents an established model to study immune responses to bacterial infection. In this investigation, we used the TUNEL (terminal deoxynucleotidyltransferase- mediated dUTP-biotin nick end labeling) technique to evaluate presence and topographic location of apoptosis-associated DNA damage in human gingival biopsies along with the expression of the p53 and Bcl-2 apoptosis-regulating proteins. Qualitative data analysis showed high densities of cells expressing DNA damage and p53 both within the epithelial attachment to the tooth and in the perivascular infiltrate (infiltrated connective tissue [ICT]) immediately underlying the site of chronic bacterial aggression. Topographic consistency between DNA damage- and p53-positive cells was consistently observed. Quantitative analysis of the ICT showed mean densities of DNA damage- and p53-positive cells of 345 ± 278 and 403 ± 182 cells/mm2, respectively. Numerical consistency was confirmed by multivariate regression analysis: densities of DNA damage-positive cells were significantly predicted by densities of p53-positive cells (P = 0.001, r2 = 0.84). In the ICT, cells displaying biotinylated DNA nicks were 3.8% ± 2.7% of total cellularity, while p53- and Bcl-2-positive cells represented 4.4% ± 1.7% and 15.4% ± 6.7% of total cells, respectively. It is suggested that p53 expression associated with DNA damage is a prevalent phenomenon in chronically inflamed human gingiva, and that apoptosis may be a relevant process for the maintenance of local immune homeostasis at sites of chronic bacterial challenge in vivo.en_US
dc.languageengen_US
dc.relation.ispartofInfection and Immunityen_US
dc.subject.meshApoptosis - Immunologyen_US
dc.subject.meshBacterial Infections - Immunology - Pathologyen_US
dc.subject.meshCell Counten_US
dc.subject.meshChronic Diseaseen_US
dc.subject.meshDna Damageen_US
dc.subject.meshGingivitis - Immunology - Microbiology - Pathologyen_US
dc.subject.meshHumansen_US
dc.subject.meshIn Situ Nick-End Labeling - Methodsen_US
dc.subject.meshKi-67 Antigen - Analysisen_US
dc.subject.meshProto-Oncogene Proteins C-Bcl-2 - Analysisen_US
dc.subject.meshTumor Suppressor Protein P53 - Analysisen_US
dc.titleIn situ detection of apoptosis at sites of chronic bacterially induced inflammation in human gingivaen_US
dc.typeArticleen_US
dc.identifier.emailLang, NP:nplang@hkucc.hku.hken_US
dc.identifier.authorityLang, NP=rp00031en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid9784521-
dc.identifier.scopuseid_2-s2.0-0032441638en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032441638&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume66en_US
dc.identifier.issue11en_US
dc.identifier.spage5190en_US
dc.identifier.epage5195en_US
dc.identifier.isiWOS:000076624800019-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridTonetti, MS=35602248900en_US
dc.identifier.scopusauthoridCortellini, D=33267525600en_US
dc.identifier.scopusauthoridLang, NP=7201577367en_US

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