Toll-like receptor 5- and lymphotoxin β receptor-dependent epithelial Ccl20 expression involves the same NF-κB binding site but distinct NF-κB pathways and dynamics

Autores
Sirard, Jean-Claude; Didierlaurent, Arnaud; Cayet, Delphine; Sierro, Frédéric; Rumbo, Martín
Año de publicación
2009
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Canonical and alternative NF-κB pathways depend on distinct NF-κB members and regulate expression of different gene subset in inflammatory and steady state conditions, respectively. In intestinal epithelial cells, both pathways control the transcription of the gene coding the CCL20 chemokine. Lymphotoxin β receptor (LTβR) mediates long lasting CCL20 expression whereas Toll-like receptor 5 (TLR5) signals promote inducible and transient activation. Here, we investigated whether the regulation of CCL20 expression involves different promoter sites and NF-κB molecules in response to TLR5 and LTβR stimulation. In epithelial cells, both stimulation required the same promoter regions, especially the NF-κB binding site but involved different NF-κB isoforms: p65/p50 and p52/RelB, for TLR5 and LTβR-dependent activation, respectively. The dynamic of activation and interaction with CCL20-specific NF-κB site correlated with gene transcription. Similar Ccl20 expression and NF-κB activation was found in the small intestine of mice stimulated with TLR5 and LTβR agonists. In summary, different NF-κB pathways modulate CCL20 transcription by operating on the same NF-κB binding site in the same cell type.
Facultad de Ciencias Exactas
Laboratorio de Investigaciones del Sistema Inmune
Materia
Ciencias Exactas
Medicina
NF-kappa-B
Toll-like receptor
Lymphotoxin beta
Chemokine
CCL20
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/128906

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repository_id_str 1329
network_name_str SEDICI (UNLP)
spelling Toll-like receptor 5- and lymphotoxin β receptor-dependent epithelial Ccl20 expression involves the same NF-κB binding site but distinct NF-κB pathways and dynamicsSirard, Jean-ClaudeDidierlaurent, ArnaudCayet, DelphineSierro, FrédéricRumbo, MartínCiencias ExactasMedicinaNF-kappa-BToll-like receptorLymphotoxin betaChemokineCCL20Canonical and alternative NF-κB pathways depend on distinct NF-κB members and regulate expression of different gene subset in inflammatory and steady state conditions, respectively. In intestinal epithelial cells, both pathways control the transcription of the gene coding the CCL20 chemokine. Lymphotoxin β receptor (LTβR) mediates long lasting CCL20 expression whereas Toll-like receptor 5 (TLR5) signals promote inducible and transient activation. Here, we investigated whether the regulation of CCL20 expression involves different promoter sites and NF-κB molecules in response to TLR5 and LTβR stimulation. In epithelial cells, both stimulation required the same promoter regions, especially the NF-κB binding site but involved different NF-κB isoforms: p65/p50 and p52/RelB, for TLR5 and LTβR-dependent activation, respectively. The dynamic of activation and interaction with CCL20-specific NF-κB site correlated with gene transcription. Similar Ccl20 expression and NF-κB activation was found in the small intestine of mice stimulated with TLR5 and LTβR agonists. In summary, different NF-κB pathways modulate CCL20 transcription by operating on the same NF-κB binding site in the same cell type.Facultad de Ciencias ExactasLaboratorio de Investigaciones del Sistema Inmune2009-05info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf386-394http://sedici.unlp.edu.ar/handle/10915/128906enginfo:eu-repo/semantics/altIdentifier/issn/0006-3002info:eu-repo/semantics/altIdentifier/pmid/19303953info:eu-repo/semantics/altIdentifier/doi/10.1016/j.bbagrm.2009.03.001info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-03T11:02:59Zoai:sedici.unlp.edu.ar:10915/128906Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-03 11:02:59.736SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Toll-like receptor 5- and lymphotoxin β receptor-dependent epithelial Ccl20 expression involves the same NF-κB binding site but distinct NF-κB pathways and dynamics
title Toll-like receptor 5- and lymphotoxin β receptor-dependent epithelial Ccl20 expression involves the same NF-κB binding site but distinct NF-κB pathways and dynamics
spellingShingle Toll-like receptor 5- and lymphotoxin β receptor-dependent epithelial Ccl20 expression involves the same NF-κB binding site but distinct NF-κB pathways and dynamics
Sirard, Jean-Claude
Ciencias Exactas
Medicina
NF-kappa-B
Toll-like receptor
Lymphotoxin beta
Chemokine
CCL20
title_short Toll-like receptor 5- and lymphotoxin β receptor-dependent epithelial Ccl20 expression involves the same NF-κB binding site but distinct NF-κB pathways and dynamics
title_full Toll-like receptor 5- and lymphotoxin β receptor-dependent epithelial Ccl20 expression involves the same NF-κB binding site but distinct NF-κB pathways and dynamics
title_fullStr Toll-like receptor 5- and lymphotoxin β receptor-dependent epithelial Ccl20 expression involves the same NF-κB binding site but distinct NF-κB pathways and dynamics
title_full_unstemmed Toll-like receptor 5- and lymphotoxin β receptor-dependent epithelial Ccl20 expression involves the same NF-κB binding site but distinct NF-κB pathways and dynamics
title_sort Toll-like receptor 5- and lymphotoxin β receptor-dependent epithelial Ccl20 expression involves the same NF-κB binding site but distinct NF-κB pathways and dynamics
dc.creator.none.fl_str_mv Sirard, Jean-Claude
Didierlaurent, Arnaud
Cayet, Delphine
Sierro, Frédéric
Rumbo, Martín
author Sirard, Jean-Claude
author_facet Sirard, Jean-Claude
Didierlaurent, Arnaud
Cayet, Delphine
Sierro, Frédéric
Rumbo, Martín
author_role author
author2 Didierlaurent, Arnaud
Cayet, Delphine
Sierro, Frédéric
Rumbo, Martín
author2_role author
author
author
author
dc.subject.none.fl_str_mv Ciencias Exactas
Medicina
NF-kappa-B
Toll-like receptor
Lymphotoxin beta
Chemokine
CCL20
topic Ciencias Exactas
Medicina
NF-kappa-B
Toll-like receptor
Lymphotoxin beta
Chemokine
CCL20
dc.description.none.fl_txt_mv Canonical and alternative NF-κB pathways depend on distinct NF-κB members and regulate expression of different gene subset in inflammatory and steady state conditions, respectively. In intestinal epithelial cells, both pathways control the transcription of the gene coding the CCL20 chemokine. Lymphotoxin β receptor (LTβR) mediates long lasting CCL20 expression whereas Toll-like receptor 5 (TLR5) signals promote inducible and transient activation. Here, we investigated whether the regulation of CCL20 expression involves different promoter sites and NF-κB molecules in response to TLR5 and LTβR stimulation. In epithelial cells, both stimulation required the same promoter regions, especially the NF-κB binding site but involved different NF-κB isoforms: p65/p50 and p52/RelB, for TLR5 and LTβR-dependent activation, respectively. The dynamic of activation and interaction with CCL20-specific NF-κB site correlated with gene transcription. Similar Ccl20 expression and NF-κB activation was found in the small intestine of mice stimulated with TLR5 and LTβR agonists. In summary, different NF-κB pathways modulate CCL20 transcription by operating on the same NF-κB binding site in the same cell type.
Facultad de Ciencias Exactas
Laboratorio de Investigaciones del Sistema Inmune
description Canonical and alternative NF-κB pathways depend on distinct NF-κB members and regulate expression of different gene subset in inflammatory and steady state conditions, respectively. In intestinal epithelial cells, both pathways control the transcription of the gene coding the CCL20 chemokine. Lymphotoxin β receptor (LTβR) mediates long lasting CCL20 expression whereas Toll-like receptor 5 (TLR5) signals promote inducible and transient activation. Here, we investigated whether the regulation of CCL20 expression involves different promoter sites and NF-κB molecules in response to TLR5 and LTβR stimulation. In epithelial cells, both stimulation required the same promoter regions, especially the NF-κB binding site but involved different NF-κB isoforms: p65/p50 and p52/RelB, for TLR5 and LTβR-dependent activation, respectively. The dynamic of activation and interaction with CCL20-specific NF-κB site correlated with gene transcription. Similar Ccl20 expression and NF-κB activation was found in the small intestine of mice stimulated with TLR5 and LTβR agonists. In summary, different NF-κB pathways modulate CCL20 transcription by operating on the same NF-κB binding site in the same cell type.
publishDate 2009
dc.date.none.fl_str_mv 2009-05
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
Articulo
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://sedici.unlp.edu.ar/handle/10915/128906
url http://sedici.unlp.edu.ar/handle/10915/128906
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/issn/0006-3002
info:eu-repo/semantics/altIdentifier/pmid/19303953
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.bbagrm.2009.03.001
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
dc.format.none.fl_str_mv application/pdf
386-394
dc.source.none.fl_str_mv reponame:SEDICI (UNLP)
instname:Universidad Nacional de La Plata
instacron:UNLP
reponame_str SEDICI (UNLP)
collection SEDICI (UNLP)
instname_str Universidad Nacional de La Plata
instacron_str UNLP
institution UNLP
repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
repository.mail.fl_str_mv alira@sedici.unlp.edu.ar
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