A preliminar analysis of the influence of Resistin on immunological cells in nonalcoholic fatty liver disease
- Autores
- Garcia, Cecilia Alejandra; Alegre, Nadia Soledad; Baz, Placida; Benavidez, Javier; Colombato, Luis; Poncino, Daniel Alberto; Garcia Daniel; Romeo, Juan Manuel; Ameigeiras, Beatriz; Cherñavsky, Alejandra Claudia
- Año de publicación
- 2016
- Idioma
- español castellano
- Tipo de recurso
- documento de conferencia
- Estado
- versión publicada
- Descripción
- Background: Resistin (RES) is a cytokine highly expressed in plasma of nonalcoholic fatty liver disease (NAFLD) patients which promotes insulin resistance. It has a pro-inflammatory role through simulation of liver/adipose infiltrating monocytes/macrophages. As these cells are the main source of RES, a pro-inflammatory loop is created due to its role as chemokine for T cells. RES binding to adenylyl cyclase-associated protein 1 (CAP1), which expression was only reported in monocytes, activates nuclear factor kappa B (NF-kB). NF-kB is also activated via TCR to modulate CD69 expression in immunological cells. Aims: to evaluate CAP1 expression in peripheral blood mononuclear cells (PBMC) from patients and controls (Co), and RES-mediated modulation of CD69. Methods: PBMC were obtained by density gradient from whole blood of NAFLD patients (n= 8) and Co (n= 10). All patients provided written informed consent. CAP1 expression was studied by flow cytometry (FC) in PBMC stained with anti-CD3, -CD4, -CD14 and -CD56 antibodies. For functional approach, PBMC from Co were stimulated with coated anti-CD3 (3ug/ml) +/- RES (500 ng/ml) for 24 h, stained with anti-CD3, -CD4 and -CD56 and evaluated for CD69 expression by FC. Mann-Whitney test was used. Results: CAP1 expression is decreased in monocytes (p=0.018), CD3+CD4+ (p=0.016) and CD3+ CD4- (p=0.018) cells in patients with NAFLD (vs. Co). RES alone did not activate PBMC. Costimulation with anti-CD3+RES decreased CD69 mean fluorescence intensity (MFI) in CD3+CD4+ and CD3+CD4-, natural killer T (NKT) and NK CD56 bright cells (p=0.0043, p=0.021, p=0.044 and p=0.035 respectively; anti-CD3+RES vs. anti-CD3). Conclusion: CAP1 is a functional receptor in healthy donors able to regulate RES influence on immunological cells. Even though RES does not induce CD69 expression per se, it can modulate the activation of immunological cells. Thus, an overall decrease in CAP1 expression might modulate the stimulus induced by RES in the context of NAFLD. This potential regulatory circuit deserves further investigation.
Fil: Garcia, Cecilia Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Fil: Alegre, Nadia Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Fil: Baz, Placida. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
Fil: Benavidez, Javier. Hospital Británico de Buenos Aires; Argentina
Fil: Colombato, Luis. Hospital Británico de Buenos Aires; Argentina
Fil: Poncino, Daniel Alberto. Sanatorio Méndez; Argentina
Fil: Garcia Daniel. Hospital Británico de Buenos Aires; Argentina
Fil: Romeo, Juan Manuel. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Ramos Mejía"; Argentina
Fil: Ameigeiras, Beatriz. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Ramos Mejía"; Argentina
Fil: Cherñavsky, Alejandra Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina
LXI Reunión Anual de la Sociedad Agentina de Investigación Clínica; LXIV Reunión Anual de la Sociedad Argentina de Inmunología; XLVIII Reunión Anual de la Sociedad Argentina de Farmacología Experimental; VII Reunión Anual de la Sociedad Argentina de Nanomedicina y V Congreso Nacional de la Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio
Mar del Plata
Argentina
Sociedad Argentina de Inmunología
Sociedad Argentina de Investigacion Clínica
Sociedad Argentina de Farmacología Experimental
Sociedad Argentina de Nanomedicina
Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio - Materia
-
RESISTIN
NAFLD - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/221481
Ver los metadatos del registro completo
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A preliminar analysis of the influence of Resistin on immunological cells in nonalcoholic fatty liver diseaseGarcia, Cecilia AlejandraAlegre, Nadia SoledadBaz, PlacidaBenavidez, JavierColombato, LuisPoncino, Daniel AlbertoGarcia DanielRomeo, Juan ManuelAmeigeiras, BeatrizCherñavsky, Alejandra ClaudiaRESISTINNAFLDhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Background: Resistin (RES) is a cytokine highly expressed in plasma of nonalcoholic fatty liver disease (NAFLD) patients which promotes insulin resistance. It has a pro-inflammatory role through simulation of liver/adipose infiltrating monocytes/macrophages. As these cells are the main source of RES, a pro-inflammatory loop is created due to its role as chemokine for T cells. RES binding to adenylyl cyclase-associated protein 1 (CAP1), which expression was only reported in monocytes, activates nuclear factor kappa B (NF-kB). NF-kB is also activated via TCR to modulate CD69 expression in immunological cells. Aims: to evaluate CAP1 expression in peripheral blood mononuclear cells (PBMC) from patients and controls (Co), and RES-mediated modulation of CD69. Methods: PBMC were obtained by density gradient from whole blood of NAFLD patients (n= 8) and Co (n= 10). All patients provided written informed consent. CAP1 expression was studied by flow cytometry (FC) in PBMC stained with anti-CD3, -CD4, -CD14 and -CD56 antibodies. For functional approach, PBMC from Co were stimulated with coated anti-CD3 (3ug/ml) +/- RES (500 ng/ml) for 24 h, stained with anti-CD3, -CD4 and -CD56 and evaluated for CD69 expression by FC. Mann-Whitney test was used. Results: CAP1 expression is decreased in monocytes (p=0.018), CD3+CD4+ (p=0.016) and CD3+ CD4- (p=0.018) cells in patients with NAFLD (vs. Co). RES alone did not activate PBMC. Costimulation with anti-CD3+RES decreased CD69 mean fluorescence intensity (MFI) in CD3+CD4+ and CD3+CD4-, natural killer T (NKT) and NK CD56 bright cells (p=0.0043, p=0.021, p=0.044 and p=0.035 respectively; anti-CD3+RES vs. anti-CD3). Conclusion: CAP1 is a functional receptor in healthy donors able to regulate RES influence on immunological cells. Even though RES does not induce CD69 expression per se, it can modulate the activation of immunological cells. Thus, an overall decrease in CAP1 expression might modulate the stimulus induced by RES in the context of NAFLD. This potential regulatory circuit deserves further investigation.Fil: Garcia, Cecilia Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFil: Alegre, Nadia Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFil: Baz, Placida. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFil: Benavidez, Javier. Hospital Británico de Buenos Aires; ArgentinaFil: Colombato, Luis. Hospital Británico de Buenos Aires; ArgentinaFil: Poncino, Daniel Alberto. Sanatorio Méndez; ArgentinaFil: Garcia Daniel. Hospital Británico de Buenos Aires; ArgentinaFil: Romeo, Juan Manuel. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Ramos Mejía"; ArgentinaFil: Ameigeiras, Beatriz. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Ramos Mejía"; ArgentinaFil: Cherñavsky, Alejandra Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaLXI Reunión Anual de la Sociedad Agentina de Investigación Clínica; LXIV Reunión Anual de la Sociedad Argentina de Inmunología; XLVIII Reunión Anual de la Sociedad Argentina de Farmacología Experimental; VII Reunión Anual de la Sociedad Argentina de Nanomedicina y V Congreso Nacional de la Asociación Argentina de Ciencia y Tecnología de Animales de LaboratorioMar del PlataArgentinaSociedad Argentina de InmunologíaSociedad Argentina de Investigacion ClínicaSociedad Argentina de Farmacología ExperimentalSociedad Argentina de NanomedicinaAsociación Argentina de Ciencia y Tecnología de Animales de LaboratorioFundación Revista Medicina2016info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/221481A preliminar analysis of the influence of Resistin on immunological cells in nonalcoholic fatty liver disease; LXI Reunión Anual de la Sociedad Agentina de Investigación Clínica; LXIV Reunión Anual de la Sociedad Argentina de Inmunología; XLVIII Reunión Anual de la Sociedad Argentina de Farmacología Experimental; VII Reunión Anual de la Sociedad Argentina de Nanomedicina y V Congreso Nacional de la Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio; Mar del Plata; Argentina; 2016; 1-61669-9106CONICET DigitalCONICETspainfo:eu-repo/semantics/altIdentifier/url/https://medicinabuenosaires.com/revistas/vol76-16/s1/92-330-RESUMENES-1-C.pdfNacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:41:07Zoai:ri.conicet.gov.ar:11336/221481instacron: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 10:41:07.483CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
A preliminar analysis of the influence of Resistin on immunological cells in nonalcoholic fatty liver disease |
| title |
A preliminar analysis of the influence of Resistin on immunological cells in nonalcoholic fatty liver disease |
| spellingShingle |
A preliminar analysis of the influence of Resistin on immunological cells in nonalcoholic fatty liver disease Garcia, Cecilia Alejandra RESISTIN NAFLD |
| title_short |
A preliminar analysis of the influence of Resistin on immunological cells in nonalcoholic fatty liver disease |
| title_full |
A preliminar analysis of the influence of Resistin on immunological cells in nonalcoholic fatty liver disease |
| title_fullStr |
A preliminar analysis of the influence of Resistin on immunological cells in nonalcoholic fatty liver disease |
| title_full_unstemmed |
A preliminar analysis of the influence of Resistin on immunological cells in nonalcoholic fatty liver disease |
| title_sort |
A preliminar analysis of the influence of Resistin on immunological cells in nonalcoholic fatty liver disease |
| dc.creator.none.fl_str_mv |
Garcia, Cecilia Alejandra Alegre, Nadia Soledad Baz, Placida Benavidez, Javier Colombato, Luis Poncino, Daniel Alberto Garcia Daniel Romeo, Juan Manuel Ameigeiras, Beatriz Cherñavsky, Alejandra Claudia |
| author |
Garcia, Cecilia Alejandra |
| author_facet |
Garcia, Cecilia Alejandra Alegre, Nadia Soledad Baz, Placida Benavidez, Javier Colombato, Luis Poncino, Daniel Alberto Garcia Daniel Romeo, Juan Manuel Ameigeiras, Beatriz Cherñavsky, Alejandra Claudia |
| author_role |
author |
| author2 |
Alegre, Nadia Soledad Baz, Placida Benavidez, Javier Colombato, Luis Poncino, Daniel Alberto Garcia Daniel Romeo, Juan Manuel Ameigeiras, Beatriz Cherñavsky, Alejandra Claudia |
| author2_role |
author author author author author author author author author |
| dc.subject.none.fl_str_mv |
RESISTIN NAFLD |
| topic |
RESISTIN NAFLD |
| 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: Resistin (RES) is a cytokine highly expressed in plasma of nonalcoholic fatty liver disease (NAFLD) patients which promotes insulin resistance. It has a pro-inflammatory role through simulation of liver/adipose infiltrating monocytes/macrophages. As these cells are the main source of RES, a pro-inflammatory loop is created due to its role as chemokine for T cells. RES binding to adenylyl cyclase-associated protein 1 (CAP1), which expression was only reported in monocytes, activates nuclear factor kappa B (NF-kB). NF-kB is also activated via TCR to modulate CD69 expression in immunological cells. Aims: to evaluate CAP1 expression in peripheral blood mononuclear cells (PBMC) from patients and controls (Co), and RES-mediated modulation of CD69. Methods: PBMC were obtained by density gradient from whole blood of NAFLD patients (n= 8) and Co (n= 10). All patients provided written informed consent. CAP1 expression was studied by flow cytometry (FC) in PBMC stained with anti-CD3, -CD4, -CD14 and -CD56 antibodies. For functional approach, PBMC from Co were stimulated with coated anti-CD3 (3ug/ml) +/- RES (500 ng/ml) for 24 h, stained with anti-CD3, -CD4 and -CD56 and evaluated for CD69 expression by FC. Mann-Whitney test was used. Results: CAP1 expression is decreased in monocytes (p=0.018), CD3+CD4+ (p=0.016) and CD3+ CD4- (p=0.018) cells in patients with NAFLD (vs. Co). RES alone did not activate PBMC. Costimulation with anti-CD3+RES decreased CD69 mean fluorescence intensity (MFI) in CD3+CD4+ and CD3+CD4-, natural killer T (NKT) and NK CD56 bright cells (p=0.0043, p=0.021, p=0.044 and p=0.035 respectively; anti-CD3+RES vs. anti-CD3). Conclusion: CAP1 is a functional receptor in healthy donors able to regulate RES influence on immunological cells. Even though RES does not induce CD69 expression per se, it can modulate the activation of immunological cells. Thus, an overall decrease in CAP1 expression might modulate the stimulus induced by RES in the context of NAFLD. This potential regulatory circuit deserves further investigation. Fil: Garcia, Cecilia Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Alegre, Nadia Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Baz, Placida. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina Fil: Benavidez, Javier. Hospital Británico de Buenos Aires; Argentina Fil: Colombato, Luis. Hospital Británico de Buenos Aires; Argentina Fil: Poncino, Daniel Alberto. Sanatorio Méndez; Argentina Fil: Garcia Daniel. Hospital Británico de Buenos Aires; Argentina Fil: Romeo, Juan Manuel. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Ramos Mejía"; Argentina Fil: Ameigeiras, Beatriz. Gobierno de la Ciudad de Buenos Aires. Hospital General de Agudos "Ramos Mejía"; Argentina Fil: Cherñavsky, Alejandra Claudia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; Argentina LXI Reunión Anual de la Sociedad Agentina de Investigación Clínica; LXIV Reunión Anual de la Sociedad Argentina de Inmunología; XLVIII Reunión Anual de la Sociedad Argentina de Farmacología Experimental; VII Reunión Anual de la Sociedad Argentina de Nanomedicina y V Congreso Nacional de la Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio Mar del Plata Argentina Sociedad Argentina de Inmunología Sociedad Argentina de Investigacion Clínica Sociedad Argentina de Farmacología Experimental Sociedad Argentina de Nanomedicina Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio |
| description |
Background: Resistin (RES) is a cytokine highly expressed in plasma of nonalcoholic fatty liver disease (NAFLD) patients which promotes insulin resistance. It has a pro-inflammatory role through simulation of liver/adipose infiltrating monocytes/macrophages. As these cells are the main source of RES, a pro-inflammatory loop is created due to its role as chemokine for T cells. RES binding to adenylyl cyclase-associated protein 1 (CAP1), which expression was only reported in monocytes, activates nuclear factor kappa B (NF-kB). NF-kB is also activated via TCR to modulate CD69 expression in immunological cells. Aims: to evaluate CAP1 expression in peripheral blood mononuclear cells (PBMC) from patients and controls (Co), and RES-mediated modulation of CD69. Methods: PBMC were obtained by density gradient from whole blood of NAFLD patients (n= 8) and Co (n= 10). All patients provided written informed consent. CAP1 expression was studied by flow cytometry (FC) in PBMC stained with anti-CD3, -CD4, -CD14 and -CD56 antibodies. For functional approach, PBMC from Co were stimulated with coated anti-CD3 (3ug/ml) +/- RES (500 ng/ml) for 24 h, stained with anti-CD3, -CD4 and -CD56 and evaluated for CD69 expression by FC. Mann-Whitney test was used. Results: CAP1 expression is decreased in monocytes (p=0.018), CD3+CD4+ (p=0.016) and CD3+ CD4- (p=0.018) cells in patients with NAFLD (vs. Co). RES alone did not activate PBMC. Costimulation with anti-CD3+RES decreased CD69 mean fluorescence intensity (MFI) in CD3+CD4+ and CD3+CD4-, natural killer T (NKT) and NK CD56 bright cells (p=0.0043, p=0.021, p=0.044 and p=0.035 respectively; anti-CD3+RES vs. anti-CD3). Conclusion: CAP1 is a functional receptor in healthy donors able to regulate RES influence on immunological cells. Even though RES does not induce CD69 expression per se, it can modulate the activation of immunological cells. Thus, an overall decrease in CAP1 expression might modulate the stimulus induced by RES in the context of NAFLD. This potential regulatory circuit deserves further investigation. |
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2016 |
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2016 |
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