Lack of TNFRI signaling enhances annexin A1 biological activity in intestinal inflammation

Autores
Sena, Angela; Pedrotti, Luciano Pablo; Barrios, Bibiana Elisabet; Cejas, Hugo; Balderramo, Domingo; Diller, Ana; Correa, Silvia Graciela
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
We evaluated whether the lack of TNF-α signaling increases mucosal levels of annexin A1 (AnxA1); the hypothesis stems from previous findings showing that TNF-α neutralization in Crohn´s disease patients up-regulates systemic AnxA1 expression. Biopsies from healthy volunteers and patients under anti-TNF-α therapy with remittent ulcerative colitis (UC) showed higher AnxA1 expression than those with active disease. We also evaluated dextran sulfate sodium (DSS)-acute colitis in TNF-α receptor 1 KO (TNFR1-/-) strain with impaired TNF-α signaling and C57BL/6 (WT) mice. Although both strains developed colitis, TNFR1-/- mice showed early clinical recovery, lower myeloperoxidase (MPO) activity and milder histopathological alterations. Colonic epithelium from control and DSS-treated TNFR1-/- mice showed intense AnxA1 expression and AnxA1+ CD4+ and CD8+ T cells were more frequent in TNFR1-/- animals, suggesting an extra supply of AnxA1. The pan antagonist of AnxA1 receptors exacerbated the colitis outcome in TNFR1-/- mice, supporting the pivotal role of AnxA1 in the early recovery. Our findings demonstrate that the TNF-α signaling reduction favors the expression and biological activity of AnxA1 in inflamed intestinal mucosa.
Fil: Sena, Angela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Pedrotti, Luciano Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Barrios, Bibiana Elisabet. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Cejas, Hugo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Balderramo, Domingo. Hospital Privado Centro Medico de Córdoba; Argentina
Fil: Diller, Ana. Hospital Privado Centro Medico de Córdoba; Argentina
Fil: Correa, Silvia Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Materia
THERAPY
DSS-INDUCED COLITIS
INFLAMMATION
GUT
EPITHELIUM
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:11336/46050
Acceder
id CONICETDig_1dd138076e773ed452e3863ba443feae
oai_identifier_str oai:ri.conicet.gov.ar:11336/46050
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Lack of TNFRI signaling enhances annexin A1 biological activity in intestinal inflammationSena, AngelaPedrotti, Luciano PabloBarrios, Bibiana ElisabetCejas, HugoBalderramo, DomingoDiller, AnaCorrea, Silvia GracielaTHERAPYDSS-INDUCED COLITISINFLAMMATIONGUTEPITHELIUMhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3We evaluated whether the lack of TNF-α signaling increases mucosal levels of annexin A1 (AnxA1); the hypothesis stems from previous findings showing that TNF-α neutralization in Crohn´s disease patients up-regulates systemic AnxA1 expression. Biopsies from healthy volunteers and patients under anti-TNF-α therapy with remittent ulcerative colitis (UC) showed higher AnxA1 expression than those with active disease. We also evaluated dextran sulfate sodium (DSS)-acute colitis in TNF-α receptor 1 KO (TNFR1-/-) strain with impaired TNF-α signaling and C57BL/6 (WT) mice. Although both strains developed colitis, TNFR1-/- mice showed early clinical recovery, lower myeloperoxidase (MPO) activity and milder histopathological alterations. Colonic epithelium from control and DSS-treated TNFR1-/- mice showed intense AnxA1 expression and AnxA1+ CD4+ and CD8+ T cells were more frequent in TNFR1-/- animals, suggesting an extra supply of AnxA1. The pan antagonist of AnxA1 receptors exacerbated the colitis outcome in TNFR1-/- mice, supporting the pivotal role of AnxA1 in the early recovery. Our findings demonstrate that the TNF-α signaling reduction favors the expression and biological activity of AnxA1 in inflamed intestinal mucosa.Fil: Sena, Angela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Pedrotti, Luciano Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Barrios, Bibiana Elisabet. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Cejas, Hugo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Balderramo, Domingo. Hospital Privado Centro Medico de Córdoba; ArgentinaFil: Diller, Ana. Hospital Privado Centro Medico de Córdoba; ArgentinaFil: Correa, Silvia Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaPergamon-Elsevier Science Ltd2015-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/46050Sena, Angela; Pedrotti, Luciano Pablo; Barrios, Bibiana Elisabet; Cejas, Hugo; Balderramo, Domingo; et al.; Lack of TNFRI signaling enhances annexin A1 biological activity in intestinal inflammation; Pergamon-Elsevier Science Ltd; Biochemical Pharmacology; 98; 3; 9-2015; 422-4310006-2952CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.bcp.2015.09.009info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S000629521500619Xinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:00:50Zoai:ri.conicet.gov.ar:11336/46050instacron: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:34982025-10-22 11:00:50.615CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Lack of TNFRI signaling enhances annexin A1 biological activity in intestinal inflammation
title Lack of TNFRI signaling enhances annexin A1 biological activity in intestinal inflammation
spellingShingle Lack of TNFRI signaling enhances annexin A1 biological activity in intestinal inflammation
Sena, Angela
THERAPY
DSS-INDUCED COLITIS
INFLAMMATION
GUT
EPITHELIUM
title_short Lack of TNFRI signaling enhances annexin A1 biological activity in intestinal inflammation
title_full Lack of TNFRI signaling enhances annexin A1 biological activity in intestinal inflammation
title_fullStr Lack of TNFRI signaling enhances annexin A1 biological activity in intestinal inflammation
title_full_unstemmed Lack of TNFRI signaling enhances annexin A1 biological activity in intestinal inflammation
title_sort Lack of TNFRI signaling enhances annexin A1 biological activity in intestinal inflammation
dc.creator.none.fl_str_mv Sena, Angela
Pedrotti, Luciano Pablo
Barrios, Bibiana Elisabet
Cejas, Hugo
Balderramo, Domingo
Diller, Ana
Correa, Silvia Graciela
author Sena, Angela
author_facet Sena, Angela
Pedrotti, Luciano Pablo
Barrios, Bibiana Elisabet
Cejas, Hugo
Balderramo, Domingo
Diller, Ana
Correa, Silvia Graciela
author_role author
author2 Pedrotti, Luciano Pablo
Barrios, Bibiana Elisabet
Cejas, Hugo
Balderramo, Domingo
Diller, Ana
Correa, Silvia Graciela
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv THERAPY
DSS-INDUCED COLITIS
INFLAMMATION
GUT
EPITHELIUM
topic THERAPY
DSS-INDUCED COLITIS
INFLAMMATION
GUT
EPITHELIUM
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv We evaluated whether the lack of TNF-α signaling increases mucosal levels of annexin A1 (AnxA1); the hypothesis stems from previous findings showing that TNF-α neutralization in Crohn´s disease patients up-regulates systemic AnxA1 expression. Biopsies from healthy volunteers and patients under anti-TNF-α therapy with remittent ulcerative colitis (UC) showed higher AnxA1 expression than those with active disease. We also evaluated dextran sulfate sodium (DSS)-acute colitis in TNF-α receptor 1 KO (TNFR1-/-) strain with impaired TNF-α signaling and C57BL/6 (WT) mice. Although both strains developed colitis, TNFR1-/- mice showed early clinical recovery, lower myeloperoxidase (MPO) activity and milder histopathological alterations. Colonic epithelium from control and DSS-treated TNFR1-/- mice showed intense AnxA1 expression and AnxA1+ CD4+ and CD8+ T cells were more frequent in TNFR1-/- animals, suggesting an extra supply of AnxA1. The pan antagonist of AnxA1 receptors exacerbated the colitis outcome in TNFR1-/- mice, supporting the pivotal role of AnxA1 in the early recovery. Our findings demonstrate that the TNF-α signaling reduction favors the expression and biological activity of AnxA1 in inflamed intestinal mucosa.
Fil: Sena, Angela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Pedrotti, Luciano Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Barrios, Bibiana Elisabet. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Cejas, Hugo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Balderramo, Domingo. Hospital Privado Centro Medico de Córdoba; Argentina
Fil: Diller, Ana. Hospital Privado Centro Medico de Córdoba; Argentina
Fil: Correa, Silvia Graciela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
description We evaluated whether the lack of TNF-α signaling increases mucosal levels of annexin A1 (AnxA1); the hypothesis stems from previous findings showing that TNF-α neutralization in Crohn´s disease patients up-regulates systemic AnxA1 expression. Biopsies from healthy volunteers and patients under anti-TNF-α therapy with remittent ulcerative colitis (UC) showed higher AnxA1 expression than those with active disease. We also evaluated dextran sulfate sodium (DSS)-acute colitis in TNF-α receptor 1 KO (TNFR1-/-) strain with impaired TNF-α signaling and C57BL/6 (WT) mice. Although both strains developed colitis, TNFR1-/- mice showed early clinical recovery, lower myeloperoxidase (MPO) activity and milder histopathological alterations. Colonic epithelium from control and DSS-treated TNFR1-/- mice showed intense AnxA1 expression and AnxA1+ CD4+ and CD8+ T cells were more frequent in TNFR1-/- animals, suggesting an extra supply of AnxA1. The pan antagonist of AnxA1 receptors exacerbated the colitis outcome in TNFR1-/- mice, supporting the pivotal role of AnxA1 in the early recovery. Our findings demonstrate that the TNF-α signaling reduction favors the expression and biological activity of AnxA1 in inflamed intestinal mucosa.
publishDate 2015
dc.date.none.fl_str_mv 2015-09
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/11336/46050
Sena, Angela; Pedrotti, Luciano Pablo; Barrios, Bibiana Elisabet; Cejas, Hugo; Balderramo, Domingo; et al.; Lack of TNFRI signaling enhances annexin A1 biological activity in intestinal inflammation; Pergamon-Elsevier Science Ltd; Biochemical Pharmacology; 98; 3; 9-2015; 422-431
0006-2952
CONICET Digital
CONICET
url http://hdl.handle.net/11336/46050
identifier_str_mv Sena, Angela; Pedrotti, Luciano Pablo; Barrios, Bibiana Elisabet; Cejas, Hugo; Balderramo, Domingo; et al.; Lack of TNFRI signaling enhances annexin A1 biological activity in intestinal inflammation; Pergamon-Elsevier Science Ltd; Biochemical Pharmacology; 98; 3; 9-2015; 422-431
0006-2952
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.bcp.2015.09.009
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S000629521500619X
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
dc.publisher.none.fl_str_mv Pergamon-Elsevier Science Ltd
publisher.none.fl_str_mv Pergamon-Elsevier Science Ltd
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
_version_ 1846781178169786368
score 12.982451

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