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Article: Protease-activated receptor 2 has pivotal roles in cellular mechanisms involved in experimental periodontitis

TitleProtease-activated receptor 2 has pivotal roles in cellular mechanisms involved in experimental periodontitis
Authors
Issue Date2010
PublisherAmerican Society for Microbiology. The Journal's website is located at http://iai.asm.org/
Citation
Infection and Immunity, 2010, v. 78 n. 2, p. 629-638 How to Cite?
AbstractThe tissue destruction seen in chronic periodontitis is commonly accepted to involve extensive upregulation of the host inflammatory response. Protease-activated receptor 2 (PAR-2)-null mice infected with Porphyromonas gingivalis did not display periodontal bone resorption in contrast to wild-type-infected and PAR-1-null-infected mice. Histological examination of tissues confirmed the lowered bone resorption in PAR-2-null mice and identified a substantial decrease in mast cells infiltrating the periodontal tissues of these mice. T cells from P. gingivalis-infected or immunized PAR-2-null mice proliferated less in response to antigen than those from wild-type animals. CD90 (Thy1.2) expression on CD4(+) and CD8(+) T-cell-receptor beta (TCRbeta) T cells was significantly (P < 0.001) decreased in antigen-immunized PAR-2-null mice compared to sham-immunized PAR-2-null mice; this was not observed in wild-type controls. T cells from infected or antigen-immunized PAR-2-null mice had a significantly different Th1/inflammatory cytokine profile from wild-type cells: in particular, gamma interferon, interleukins (interleukin-2, -3, and -17), granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha demonstrated lower expression than wild-type controls. The absence of PAR-2 therefore appears to substantially decrease T-cell activation and the Th1/inflammatory response. Regulation of such proinflammatory mechanisms in T cells and mast cells by PAR-2 suggests a pivotal role in the pathogenesis of the disease.
Persistent Identifierhttp://hdl.handle.net/10722/164452
ISSN
2015 Impact Factor: 3.603
2015 SCImago Journal Rankings: 2.342
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWong, DMen_US
dc.contributor.authorTam, Ven_US
dc.contributor.authorLam, Ren_US
dc.contributor.authorWalsh, KAen_US
dc.contributor.authorTatarczuch, Len_US
dc.contributor.authorPagel, CNen_US
dc.contributor.authorReynolds, ECen_US
dc.contributor.authorO'Brien-Simpson, NMen_US
dc.contributor.authorMackie, EJen_US
dc.contributor.authorPike, RNen_US
dc.date.accessioned2012-09-20T07:59:40Z-
dc.date.available2012-09-20T07:59:40Z-
dc.date.issued2010en_US
dc.identifier.citationInfection and Immunity, 2010, v. 78 n. 2, p. 629-638en_US
dc.identifier.issn0019-9567-
dc.identifier.urihttp://hdl.handle.net/10722/164452-
dc.description.abstractThe tissue destruction seen in chronic periodontitis is commonly accepted to involve extensive upregulation of the host inflammatory response. Protease-activated receptor 2 (PAR-2)-null mice infected with Porphyromonas gingivalis did not display periodontal bone resorption in contrast to wild-type-infected and PAR-1-null-infected mice. Histological examination of tissues confirmed the lowered bone resorption in PAR-2-null mice and identified a substantial decrease in mast cells infiltrating the periodontal tissues of these mice. T cells from P. gingivalis-infected or immunized PAR-2-null mice proliferated less in response to antigen than those from wild-type animals. CD90 (Thy1.2) expression on CD4(+) and CD8(+) T-cell-receptor beta (TCRbeta) T cells was significantly (P < 0.001) decreased in antigen-immunized PAR-2-null mice compared to sham-immunized PAR-2-null mice; this was not observed in wild-type controls. T cells from infected or antigen-immunized PAR-2-null mice had a significantly different Th1/inflammatory cytokine profile from wild-type cells: in particular, gamma interferon, interleukins (interleukin-2, -3, and -17), granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha demonstrated lower expression than wild-type controls. The absence of PAR-2 therefore appears to substantially decrease T-cell activation and the Th1/inflammatory response. Regulation of such proinflammatory mechanisms in T cells and mast cells by PAR-2 suggests a pivotal role in the pathogenesis of the disease.-
dc.languageengen_US
dc.publisherAmerican Society for Microbiology. The Journal's website is located at http://iai.asm.org/-
dc.relation.ispartofInfection and Immunityen_US
dc.rightsInfection and Immunity. Copyright © American Society for Microbiology.-
dc.subject.meshAlveolar Bone Loss - immunology - pathology-
dc.subject.meshCytokines - immunology-
dc.subject.meshPeriodontitis - immunology - pathology-
dc.subject.meshReceptor, PAR-2 - immunology-
dc.subject.meshT-Lymphocytes - immunology-
dc.titleProtease-activated receptor 2 has pivotal roles in cellular mechanisms involved in experimental periodontitisen_US
dc.typeArticleen_US
dc.identifier.emailTam, V: vivtam@hku.hken_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/IAI.01019-09-
dc.identifier.pmid19933835-
dc.identifier.pmcidPMC2812191-
dc.identifier.scopuseid_2-s2.0-76749083449-
dc.identifier.hkuros210235en_US
dc.identifier.volume78en_US
dc.identifier.issue2-
dc.identifier.spage629en_US
dc.identifier.epage638en_US
dc.identifier.isiWOS:000273855600008-
dc.publisher.placeUnited States-

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