Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulation

Autores
Santucci, Natalia Estefanía; Díaz, Ariana; Bianchi Fontemachi, Jose Ernesto; Spinelli, Silvana Virginia; D'attilio, Luciano David; Bongiovanni, Bettina; Dídoli, Griselda; Brandan, Nadia; Nannini, Luis; Bay, Maria Luisa; Bottasso, Oscar Adelmo
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
BACKGROUND: Tuberculosis (TB) is a infectious disease characterised by a profound immune-endocrine metabolic imbalance, including a diminution in leptin plasma levels. Leptin appears to be the link between nutritional status and the development of a protective immune response. OBJECTIVE: To examine the effects of leptin on the proliferation and production of interferon-gamma (IFN-c) by peripheral blood mononuclear cells (PBMC) in TB patients and healthy controls stimulated with mycobacterial antigens with or without leptin. As macrophages are key cells in mycobacterial containment, the effect of leptin on the production of interleukin (IL) 1b and IL-1Ra by the monocytic cell line THP-1 was also studied. RESULTS: Leptin diminished the proliferative capacity of PBMC on mycobacterial stimulation, and had no effect on IFN-c production in terms of measurements in culture supernatants or intracytoplasmic analysis using flow cytometry. Real-time polymerase chain reaction studies of PBMC from TB patients revealed a preserved expression of leptin receptor. Furthermore, IL-1b and IL- 1Ra secretion by THP-1 cells was not modified by leptin treatment. CONCLUSION: The study results do not support the utility of treatment with leptin to correct immune imbalances due to TB.
Fil: Santucci, Natalia Estefanía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Díaz, Ariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Bianchi Fontemachi, Jose Ernesto. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Spinelli, Silvana Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: D'attilio, Luciano David. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Bongiovanni, Bettina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Dídoli, Griselda. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Brandan, Nadia. Hospital Escuela Eva Perón; Argentina
Fil: Nannini, Luis. Hospital Escuela Eva Perón; Argentina
Fil: Bay, Maria Luisa. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Bottasso, Oscar Adelmo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Materia
Adipocytokines
Cytokines
Immunomodulation
Pulmonary Tuberculosis
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:11336/30113
Acceder
id CONICETDig_03a1a37092c5301f432c8e7103d28bcc
oai_identifier_str oai:ri.conicet.gov.ar:11336/30113
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulationSantucci, Natalia EstefaníaDíaz, ArianaBianchi Fontemachi, Jose ErnestoSpinelli, Silvana VirginiaD'attilio, Luciano DavidBongiovanni, BettinaDídoli, GriseldaBrandan, NadiaNannini, LuisBay, Maria LuisaBottasso, Oscar AdelmoAdipocytokinesCytokinesImmunomodulationPulmonary Tuberculosishttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3BACKGROUND: Tuberculosis (TB) is a infectious disease characterised by a profound immune-endocrine metabolic imbalance, including a diminution in leptin plasma levels. Leptin appears to be the link between nutritional status and the development of a protective immune response. OBJECTIVE: To examine the effects of leptin on the proliferation and production of interferon-gamma (IFN-c) by peripheral blood mononuclear cells (PBMC) in TB patients and healthy controls stimulated with mycobacterial antigens with or without leptin. As macrophages are key cells in mycobacterial containment, the effect of leptin on the production of interleukin (IL) 1b and IL-1Ra by the monocytic cell line THP-1 was also studied. RESULTS: Leptin diminished the proliferative capacity of PBMC on mycobacterial stimulation, and had no effect on IFN-c production in terms of measurements in culture supernatants or intracytoplasmic analysis using flow cytometry. Real-time polymerase chain reaction studies of PBMC from TB patients revealed a preserved expression of leptin receptor. Furthermore, IL-1b and IL- 1Ra secretion by THP-1 cells was not modified by leptin treatment. CONCLUSION: The study results do not support the utility of treatment with leptin to correct immune imbalances due to TB.Fil: Santucci, Natalia Estefanía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; ArgentinaFil: Díaz, Ariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; ArgentinaFil: Bianchi Fontemachi, Jose Ernesto. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; ArgentinaFil: Spinelli, Silvana Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; ArgentinaFil: D'attilio, Luciano David. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; ArgentinaFil: Bongiovanni, Bettina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; ArgentinaFil: Dídoli, Griselda. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; ArgentinaFil: Brandan, Nadia. Hospital Escuela Eva Perón; ArgentinaFil: Nannini, Luis. Hospital Escuela Eva Perón; ArgentinaFil: Bay, Maria Luisa. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; ArgentinaFil: Bottasso, Oscar Adelmo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; ArgentinaInternational Union Against Tuberculosis and Lung Disease2014-08info: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/11336/30113Santucci, Natalia Estefanía; Díaz, Ariana; Bianchi Fontemachi, Jose Ernesto; Spinelli, Silvana Virginia; D'attilio, Luciano David; et al.; Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulation; International Union Against Tuberculosis and Lung Disease; International Journal of Tuberculosis and Lung Disease; 18; 8; 8-2014; 981-9871027-3719CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.5588/ijtld.13.0780info:eu-repo/semantics/altIdentifier/url/http://www.ingentaconnect.com/content/iuatld/ijtld/2014/00000018/00000008/art00019info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:54:09Zoai:ri.conicet.gov.ar:11336/30113instacron: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 09:54:09.959CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulation
title Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulation
spellingShingle Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulation
Santucci, Natalia Estefanía
Adipocytokines
Cytokines
Immunomodulation
Pulmonary Tuberculosis
title_short Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulation
title_full Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulation
title_fullStr Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulation
title_full_unstemmed Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulation
title_sort Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulation
dc.creator.none.fl_str_mv Santucci, Natalia Estefanía
Díaz, Ariana
Bianchi Fontemachi, Jose Ernesto
Spinelli, Silvana Virginia
D'attilio, Luciano David
Bongiovanni, Bettina
Dídoli, Griselda
Brandan, Nadia
Nannini, Luis
Bay, Maria Luisa
Bottasso, Oscar Adelmo
author Santucci, Natalia Estefanía
author_facet Santucci, Natalia Estefanía
Díaz, Ariana
Bianchi Fontemachi, Jose Ernesto
Spinelli, Silvana Virginia
D'attilio, Luciano David
Bongiovanni, Bettina
Dídoli, Griselda
Brandan, Nadia
Nannini, Luis
Bay, Maria Luisa
Bottasso, Oscar Adelmo
author_role author
author2 Díaz, Ariana
Bianchi Fontemachi, Jose Ernesto
Spinelli, Silvana Virginia
D'attilio, Luciano David
Bongiovanni, Bettina
Dídoli, Griselda
Brandan, Nadia
Nannini, Luis
Bay, Maria Luisa
Bottasso, Oscar Adelmo
author2_role author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Adipocytokines
Cytokines
Immunomodulation
Pulmonary Tuberculosis
topic Adipocytokines
Cytokines
Immunomodulation
Pulmonary Tuberculosis
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: Tuberculosis (TB) is a infectious disease characterised by a profound immune-endocrine metabolic imbalance, including a diminution in leptin plasma levels. Leptin appears to be the link between nutritional status and the development of a protective immune response. OBJECTIVE: To examine the effects of leptin on the proliferation and production of interferon-gamma (IFN-c) by peripheral blood mononuclear cells (PBMC) in TB patients and healthy controls stimulated with mycobacterial antigens with or without leptin. As macrophages are key cells in mycobacterial containment, the effect of leptin on the production of interleukin (IL) 1b and IL-1Ra by the monocytic cell line THP-1 was also studied. RESULTS: Leptin diminished the proliferative capacity of PBMC on mycobacterial stimulation, and had no effect on IFN-c production in terms of measurements in culture supernatants or intracytoplasmic analysis using flow cytometry. Real-time polymerase chain reaction studies of PBMC from TB patients revealed a preserved expression of leptin receptor. Furthermore, IL-1b and IL- 1Ra secretion by THP-1 cells was not modified by leptin treatment. CONCLUSION: The study results do not support the utility of treatment with leptin to correct immune imbalances due to TB.
Fil: Santucci, Natalia Estefanía. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Díaz, Ariana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Bianchi Fontemachi, Jose Ernesto. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Spinelli, Silvana Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: D'attilio, Luciano David. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Bongiovanni, Bettina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Dídoli, Griselda. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Brandan, Nadia. Hospital Escuela Eva Perón; Argentina
Fil: Nannini, Luis. Hospital Escuela Eva Perón; Argentina
Fil: Bay, Maria Luisa. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
Fil: Bottasso, Oscar Adelmo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario; Argentina. Universidad Nacional de Rosario. Facultad de Ciencias Médicas. Instituto de Inmunología; Argentina
description BACKGROUND: Tuberculosis (TB) is a infectious disease characterised by a profound immune-endocrine metabolic imbalance, including a diminution in leptin plasma levels. Leptin appears to be the link between nutritional status and the development of a protective immune response. OBJECTIVE: To examine the effects of leptin on the proliferation and production of interferon-gamma (IFN-c) by peripheral blood mononuclear cells (PBMC) in TB patients and healthy controls stimulated with mycobacterial antigens with or without leptin. As macrophages are key cells in mycobacterial containment, the effect of leptin on the production of interleukin (IL) 1b and IL-1Ra by the monocytic cell line THP-1 was also studied. RESULTS: Leptin diminished the proliferative capacity of PBMC on mycobacterial stimulation, and had no effect on IFN-c production in terms of measurements in culture supernatants or intracytoplasmic analysis using flow cytometry. Real-time polymerase chain reaction studies of PBMC from TB patients revealed a preserved expression of leptin receptor. Furthermore, IL-1b and IL- 1Ra secretion by THP-1 cells was not modified by leptin treatment. CONCLUSION: The study results do not support the utility of treatment with leptin to correct immune imbalances due to TB.
publishDate 2014
dc.date.none.fl_str_mv 2014-08
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/11336/30113
Santucci, Natalia Estefanía; Díaz, Ariana; Bianchi Fontemachi, Jose Ernesto; Spinelli, Silvana Virginia; D'attilio, Luciano David; et al.; Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulation; International Union Against Tuberculosis and Lung Disease; International Journal of Tuberculosis and Lung Disease; 18; 8; 8-2014; 981-987
1027-3719
CONICET Digital
CONICET
url http://hdl.handle.net/11336/30113
identifier_str_mv Santucci, Natalia Estefanía; Díaz, Ariana; Bianchi Fontemachi, Jose Ernesto; Spinelli, Silvana Virginia; D'attilio, Luciano David; et al.; Leptin does not enhance cell-mediated immune responses following mycobacterial antigen stimulation; International Union Against Tuberculosis and Lung Disease; International Journal of Tuberculosis and Lung Disease; 18; 8; 8-2014; 981-987
1027-3719
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.5588/ijtld.13.0780
info:eu-repo/semantics/altIdentifier/url/http://www.ingentaconnect.com/content/iuatld/ijtld/2014/00000018/00000008/art00019
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
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv International Union Against Tuberculosis and Lung Disease
publisher.none.fl_str_mv International Union Against Tuberculosis and Lung Disease
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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