Autoantibodies to β1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger PGE2 generation

Autores
Sterin, Leonor Josefina; Furlan, César; Borda, Enri Santiago
Año de publicación
2009
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Background and Objective: Autoimmune mechanisms may contribute to the pathogenesis of periodontal disease. Autoantibodies with the potential to bind and activate b1 -adrenoceptors (b1 -AR) of human gingival fibroblasts were studied to provide evidence of altered humoral immune response in chronic periodontal 2disease. Material and Methods: Flow cytometry and enzyme-linked immunosorbent assay using cell culture-adherent gingival fibroblasts and/or their purified membranes and/or a synthetic peptide corresponding to the second extracellular loop of human b1-AR were used to detect serum antibodies. The effects of antibodies from chronic periodontal disease patients on PGE2 generation and CD40 expression were also tested. Results: Circulating immunoglobulin G (IgG) from chronic periodontal disease patients (but not from normal individuals) interacted with the fibroblast surface, 3activating b1-AR. Atenolol or CGP 20712 and b1 synthetic peptide inhibited the 4interaction of IgG with b1-AR. Immunoglobulin G from chronic periodontal disease patients also displayed agonist-like activity associated with specific b1-AR activation, increasing PGE2 generation and CD40 overexpression. The corresponding affinity-purified anti-b1 -AR peptide IgG mimicked these effects. Both effects were prevented by inhibition of cyclo-oxygenase. Conclusion: This article supports the participation of humoral immune alterations in chronic periodontal disease resulting in postsynaptic functional deregulation. Overproduction of proinflammatory mediators (PGE2 and CD40 expression) is induced as a consequence of antibody–b1 -AR interaction. The PGE2–CD40–IgG 5axis may play a part in the pathophysiological mechanisms underlying the inflammatory process in chronic periodontal disease.
Fil: Sterin, Leonor Josefina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
Fil: Furlan, César. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
Fil: Borda, Enri Santiago. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
Materia
Autoantibodies
b-adrenoceptors
CD40 expression
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/157659
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/157659
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Autoantibodies to β1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger PGE2 generationSterin, Leonor JosefinaFurlan, CésarBorda, Enri SantiagoAutoantibodiesb-adrenoceptorsCD40 expressionhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Background and Objective: Autoimmune mechanisms may contribute to the pathogenesis of periodontal disease. Autoantibodies with the potential to bind and activate b1 -adrenoceptors (b1 -AR) of human gingival fibroblasts were studied to provide evidence of altered humoral immune response in chronic periodontal 2disease. Material and Methods: Flow cytometry and enzyme-linked immunosorbent assay using cell culture-adherent gingival fibroblasts and/or their purified membranes and/or a synthetic peptide corresponding to the second extracellular loop of human b1-AR were used to detect serum antibodies. The effects of antibodies from chronic periodontal disease patients on PGE2 generation and CD40 expression were also tested. Results: Circulating immunoglobulin G (IgG) from chronic periodontal disease patients (but not from normal individuals) interacted with the fibroblast surface, 3activating b1-AR. Atenolol or CGP 20712 and b1 synthetic peptide inhibited the 4interaction of IgG with b1-AR. Immunoglobulin G from chronic periodontal disease patients also displayed agonist-like activity associated with specific b1-AR activation, increasing PGE2 generation and CD40 overexpression. The corresponding affinity-purified anti-b1 -AR peptide IgG mimicked these effects. Both effects were prevented by inhibition of cyclo-oxygenase. Conclusion: This article supports the participation of humoral immune alterations in chronic periodontal disease resulting in postsynaptic functional deregulation. Overproduction of proinflammatory mediators (PGE2 and CD40 expression) is induced as a consequence of antibody–b1 -AR interaction. The PGE2–CD40–IgG 5axis may play a part in the pathophysiological mechanisms underlying the inflammatory process in chronic periodontal disease.Fil: Sterin, Leonor Josefina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; ArgentinaFil: Furlan, César. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; ArgentinaFil: Borda, Enri Santiago. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; ArgentinaWiley Blackwell Publishing, Inc2009-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/157659Sterin, Leonor Josefina; Furlan, César; Borda, Enri Santiago; Autoantibodies to β1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger PGE2 generation; Wiley Blackwell Publishing, Inc; Journal of Periodontal Research; 44; 4; 6-2009; 330-3370022-34841600-0765CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/10.1111/j.1600-0765.2008.01139.xinfo:eu-repo/semantics/altIdentifier/doi/10.1111/j.1600-0765.2008.01139.xinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:04:45Zoai:ri.conicet.gov.ar:11336/157659instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:04:46.21CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Autoantibodies to β1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger PGE2 generation
title Autoantibodies to β1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger PGE2 generation
spellingShingle Autoantibodies to β1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger PGE2 generation
Sterin, Leonor Josefina
Autoantibodies
b-adrenoceptors
CD40 expression
title_short Autoantibodies to β1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger PGE2 generation
title_full Autoantibodies to β1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger PGE2 generation
title_fullStr Autoantibodies to β1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger PGE2 generation
title_full_unstemmed Autoantibodies to β1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger PGE2 generation
title_sort Autoantibodies to β1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger PGE2 generation
dc.creator.none.fl_str_mv Sterin, Leonor Josefina
Furlan, César
Borda, Enri Santiago
author Sterin, Leonor Josefina
author_facet Sterin, Leonor Josefina
Furlan, César
Borda, Enri Santiago
author_role author
author2 Furlan, César
Borda, Enri Santiago
author2_role author
author
dc.subject.none.fl_str_mv Autoantibodies
b-adrenoceptors
CD40 expression
topic Autoantibodies
b-adrenoceptors
CD40 expression
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Background and Objective: Autoimmune mechanisms may contribute to the pathogenesis of periodontal disease. Autoantibodies with the potential to bind and activate b1 -adrenoceptors (b1 -AR) of human gingival fibroblasts were studied to provide evidence of altered humoral immune response in chronic periodontal 2disease. Material and Methods: Flow cytometry and enzyme-linked immunosorbent assay using cell culture-adherent gingival fibroblasts and/or their purified membranes and/or a synthetic peptide corresponding to the second extracellular loop of human b1-AR were used to detect serum antibodies. The effects of antibodies from chronic periodontal disease patients on PGE2 generation and CD40 expression were also tested. Results: Circulating immunoglobulin G (IgG) from chronic periodontal disease patients (but not from normal individuals) interacted with the fibroblast surface, 3activating b1-AR. Atenolol or CGP 20712 and b1 synthetic peptide inhibited the 4interaction of IgG with b1-AR. Immunoglobulin G from chronic periodontal disease patients also displayed agonist-like activity associated with specific b1-AR activation, increasing PGE2 generation and CD40 overexpression. The corresponding affinity-purified anti-b1 -AR peptide IgG mimicked these effects. Both effects were prevented by inhibition of cyclo-oxygenase. Conclusion: This article supports the participation of humoral immune alterations in chronic periodontal disease resulting in postsynaptic functional deregulation. Overproduction of proinflammatory mediators (PGE2 and CD40 expression) is induced as a consequence of antibody–b1 -AR interaction. The PGE2–CD40–IgG 5axis may play a part in the pathophysiological mechanisms underlying the inflammatory process in chronic periodontal disease.
Fil: Sterin, Leonor Josefina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
Fil: Furlan, César. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
Fil: Borda, Enri Santiago. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Odontología. Cátedra de Farmacología; Argentina
description Background and Objective: Autoimmune mechanisms may contribute to the pathogenesis of periodontal disease. Autoantibodies with the potential to bind and activate b1 -adrenoceptors (b1 -AR) of human gingival fibroblasts were studied to provide evidence of altered humoral immune response in chronic periodontal 2disease. Material and Methods: Flow cytometry and enzyme-linked immunosorbent assay using cell culture-adherent gingival fibroblasts and/or their purified membranes and/or a synthetic peptide corresponding to the second extracellular loop of human b1-AR were used to detect serum antibodies. The effects of antibodies from chronic periodontal disease patients on PGE2 generation and CD40 expression were also tested. Results: Circulating immunoglobulin G (IgG) from chronic periodontal disease patients (but not from normal individuals) interacted with the fibroblast surface, 3activating b1-AR. Atenolol or CGP 20712 and b1 synthetic peptide inhibited the 4interaction of IgG with b1-AR. Immunoglobulin G from chronic periodontal disease patients also displayed agonist-like activity associated with specific b1-AR activation, increasing PGE2 generation and CD40 overexpression. The corresponding affinity-purified anti-b1 -AR peptide IgG mimicked these effects. Both effects were prevented by inhibition of cyclo-oxygenase. Conclusion: This article supports the participation of humoral immune alterations in chronic periodontal disease resulting in postsynaptic functional deregulation. Overproduction of proinflammatory mediators (PGE2 and CD40 expression) is induced as a consequence of antibody–b1 -AR interaction. The PGE2–CD40–IgG 5axis may play a part in the pathophysiological mechanisms underlying the inflammatory process in chronic periodontal disease.
publishDate 2009
dc.date.none.fl_str_mv 2009-06
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/157659
Sterin, Leonor Josefina; Furlan, César; Borda, Enri Santiago; Autoantibodies to β1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger PGE2 generation; Wiley Blackwell Publishing, Inc; Journal of Periodontal Research; 44; 4; 6-2009; 330-337
0022-3484
1600-0765
CONICET Digital
CONICET
url http://hdl.handle.net/11336/157659
identifier_str_mv Sterin, Leonor Josefina; Furlan, César; Borda, Enri Santiago; Autoantibodies to β1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger PGE2 generation; Wiley Blackwell Publishing, Inc; Journal of Periodontal Research; 44; 4; 6-2009; 330-337
0022-3484
1600-0765
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/10.1111/j.1600-0765.2008.01139.x
info:eu-repo/semantics/altIdentifier/doi/10.1111/j.1600-0765.2008.01139.x
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
publisher.none.fl_str_mv Wiley Blackwell Publishing, Inc
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.070432

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