VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophages

Autores
Larocca, Luciana; Calafat, Mario Jose; Roca, Valeria Ines; Franchi, Ana Maria; Perez Leiros, Claudia
Año de publicación
2007
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The spontaneous non obese diabetic (NOD) mouse model of Sjögren's syndrome provides a valuable tool to study the onset and progression of both autoimmune response and secretory dysfunction. Vasoactive intestinal peptide (VIP) is a neuro and immunopeptide with prosecretory effect in salivary glands and anti-inflammatory actions in various models of autoimmune disease. Our purpose was to analyze the response of peritoneal macrophages to an inflammatory stimulus during the decline of salivary secretion in NOD mice and the potential anti-inflammatory effect of VIP. We present evidence of an increased nitric oxide production by peritoneal macrophages of NOD mice in basal and lipopolysaccharide (LPS) + IFN-γ-stimulated conditions and a lower IL-10 response to LPS compared with normal BALB/c mice. VIP inhibited LPS-induced TNF-α, IL-12 and nitrites accumulation in NOD macrophages while it increased IL-10 production. VIP effect was prevented by an anti-IL-10 monoclonal antibody and it showed an additive effect on exogenously added IL-10 only in NOD mice. The inhibitory effect of VIP-induced IL-10 on nitrites was mediated by COX metabolites mostly in NOD cells as indomethacine inhibited both the increase in IL-10 and the reduction of nitrites exerted by VIP. We conclude that both PGE2 and VIP inhibit nitric oxide production and increase IL-10 induced by LPS in NOD macrophages and VIP effect is mediated through an increase of COX metabolites and IL-10.
Fil: Larocca, Luciana. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Calafat, Mario Jose. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Roca, Valeria Ines. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Franchi, Ana Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Perez Leiros, Claudia. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Materia
Il-10
Macrophages
Nitric Oxide
Nod Mice
Pge2
Vip
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/37289

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oai_identifier_str oai:ri.conicet.gov.ar:11336/37289
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network_name_str CONICET Digital (CONICET)
spelling VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophagesLarocca, LucianaCalafat, Mario JoseRoca, Valeria InesFranchi, Ana MariaPerez Leiros, ClaudiaIl-10MacrophagesNitric OxideNod MicePge2Viphttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3The spontaneous non obese diabetic (NOD) mouse model of Sjögren's syndrome provides a valuable tool to study the onset and progression of both autoimmune response and secretory dysfunction. Vasoactive intestinal peptide (VIP) is a neuro and immunopeptide with prosecretory effect in salivary glands and anti-inflammatory actions in various models of autoimmune disease. Our purpose was to analyze the response of peritoneal macrophages to an inflammatory stimulus during the decline of salivary secretion in NOD mice and the potential anti-inflammatory effect of VIP. We present evidence of an increased nitric oxide production by peritoneal macrophages of NOD mice in basal and lipopolysaccharide (LPS) + IFN-γ-stimulated conditions and a lower IL-10 response to LPS compared with normal BALB/c mice. VIP inhibited LPS-induced TNF-α, IL-12 and nitrites accumulation in NOD macrophages while it increased IL-10 production. VIP effect was prevented by an anti-IL-10 monoclonal antibody and it showed an additive effect on exogenously added IL-10 only in NOD mice. The inhibitory effect of VIP-induced IL-10 on nitrites was mediated by COX metabolites mostly in NOD cells as indomethacine inhibited both the increase in IL-10 and the reduction of nitrites exerted by VIP. We conclude that both PGE2 and VIP inhibit nitric oxide production and increase IL-10 induced by LPS in NOD macrophages and VIP effect is mediated through an increase of COX metabolites and IL-10.Fil: Larocca, Luciana. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Calafat, Mario Jose. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Roca, Valeria Ines. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Franchi, Ana Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; ArgentinaFil: Perez Leiros, Claudia. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaElsevier Science2007-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/37289Larocca, Luciana; Calafat, Mario Jose; Roca, Valeria Ines; Franchi, Ana Maria; Perez Leiros, Claudia; VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophages; Elsevier Science; International Immunopharmacology; 7; 10; 10-2007; 1343-13491567-5769CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.intimp.2007.05.017info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S1567576907001567info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:10:45Zoai:ri.conicet.gov.ar:11336/37289instacron: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:34982025-09-03 10:10:47.148CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophages
title VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophages
spellingShingle VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophages
Larocca, Luciana
Il-10
Macrophages
Nitric Oxide
Nod Mice
Pge2
Vip
title_short VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophages
title_full VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophages
title_fullStr VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophages
title_full_unstemmed VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophages
title_sort VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophages
dc.creator.none.fl_str_mv Larocca, Luciana
Calafat, Mario Jose
Roca, Valeria Ines
Franchi, Ana Maria
Perez Leiros, Claudia
author Larocca, Luciana
author_facet Larocca, Luciana
Calafat, Mario Jose
Roca, Valeria Ines
Franchi, Ana Maria
Perez Leiros, Claudia
author_role author
author2 Calafat, Mario Jose
Roca, Valeria Ines
Franchi, Ana Maria
Perez Leiros, Claudia
author2_role author
author
author
author
dc.subject.none.fl_str_mv Il-10
Macrophages
Nitric Oxide
Nod Mice
Pge2
Vip
topic Il-10
Macrophages
Nitric Oxide
Nod Mice
Pge2
Vip
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The spontaneous non obese diabetic (NOD) mouse model of Sjögren's syndrome provides a valuable tool to study the onset and progression of both autoimmune response and secretory dysfunction. Vasoactive intestinal peptide (VIP) is a neuro and immunopeptide with prosecretory effect in salivary glands and anti-inflammatory actions in various models of autoimmune disease. Our purpose was to analyze the response of peritoneal macrophages to an inflammatory stimulus during the decline of salivary secretion in NOD mice and the potential anti-inflammatory effect of VIP. We present evidence of an increased nitric oxide production by peritoneal macrophages of NOD mice in basal and lipopolysaccharide (LPS) + IFN-γ-stimulated conditions and a lower IL-10 response to LPS compared with normal BALB/c mice. VIP inhibited LPS-induced TNF-α, IL-12 and nitrites accumulation in NOD macrophages while it increased IL-10 production. VIP effect was prevented by an anti-IL-10 monoclonal antibody and it showed an additive effect on exogenously added IL-10 only in NOD mice. The inhibitory effect of VIP-induced IL-10 on nitrites was mediated by COX metabolites mostly in NOD cells as indomethacine inhibited both the increase in IL-10 and the reduction of nitrites exerted by VIP. We conclude that both PGE2 and VIP inhibit nitric oxide production and increase IL-10 induced by LPS in NOD macrophages and VIP effect is mediated through an increase of COX metabolites and IL-10.
Fil: Larocca, Luciana. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Calafat, Mario Jose. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Roca, Valeria Ines. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Franchi, Ana Maria. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos. Universidad de Buenos Aires. Facultad de Medicina. Centro de Estudios Farmacológicos y Botánicos; Argentina
Fil: Perez Leiros, Claudia. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
description The spontaneous non obese diabetic (NOD) mouse model of Sjögren's syndrome provides a valuable tool to study the onset and progression of both autoimmune response and secretory dysfunction. Vasoactive intestinal peptide (VIP) is a neuro and immunopeptide with prosecretory effect in salivary glands and anti-inflammatory actions in various models of autoimmune disease. Our purpose was to analyze the response of peritoneal macrophages to an inflammatory stimulus during the decline of salivary secretion in NOD mice and the potential anti-inflammatory effect of VIP. We present evidence of an increased nitric oxide production by peritoneal macrophages of NOD mice in basal and lipopolysaccharide (LPS) + IFN-γ-stimulated conditions and a lower IL-10 response to LPS compared with normal BALB/c mice. VIP inhibited LPS-induced TNF-α, IL-12 and nitrites accumulation in NOD macrophages while it increased IL-10 production. VIP effect was prevented by an anti-IL-10 monoclonal antibody and it showed an additive effect on exogenously added IL-10 only in NOD mice. The inhibitory effect of VIP-induced IL-10 on nitrites was mediated by COX metabolites mostly in NOD cells as indomethacine inhibited both the increase in IL-10 and the reduction of nitrites exerted by VIP. We conclude that both PGE2 and VIP inhibit nitric oxide production and increase IL-10 induced by LPS in NOD macrophages and VIP effect is mediated through an increase of COX metabolites and IL-10.
publishDate 2007
dc.date.none.fl_str_mv 2007-10
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/11336/37289
Larocca, Luciana; Calafat, Mario Jose; Roca, Valeria Ines; Franchi, Ana Maria; Perez Leiros, Claudia; VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophages; Elsevier Science; International Immunopharmacology; 7; 10; 10-2007; 1343-1349
1567-5769
CONICET Digital
CONICET
url http://hdl.handle.net/11336/37289
identifier_str_mv Larocca, Luciana; Calafat, Mario Jose; Roca, Valeria Ines; Franchi, Ana Maria; Perez Leiros, Claudia; VIP limits LPS-induced nitric oxide production through IL-10 in NOD mice macrophages; Elsevier Science; International Immunopharmacology; 7; 10; 10-2007; 1343-1349
1567-5769
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.intimp.2007.05.017
info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/pii/S1567576907001567
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Science
publisher.none.fl_str_mv Elsevier Science
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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