The Impact of IFN-g; Receptor on SLPI Expression in Active Tuberculosis: Association with Disease Severity
- Autores
- Tateosian, Nancy Liliana; Pasquinelli, Virginia; Hernández Del Pino, Rodrigo Emanuel; Ambrosi, Nella Gabriela; Guerrieri, Diego; Pedraza Sánchez, Sigifredo; Santucci, Natalia Estefanía; D'attilio, Luciano David; Pellegrini, Joaquín Miguel; Araujo Solis, María A.; Musella, Rosa M.; Palmero, Domingo J.; Hernandez Pando, Rogelio; Garcia, Veronica Edith; Chuluyan, Hector Eduardo
- Año de publicación
- 2014
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Interferon (IFN)-g displays a critical role in tuberculosis (TB), modulating the innate and adaptive immune responses. Previously, we reported that secretory leukocyte protease inhibitor (SLPI) is a pattern recognition receptor with anti-mycobacterial activity against Mycobacterium tuberculosis (Mtb). Herein, we determined whether IFN-g modulated the levels of SLPI in TB patients. Plasma levels of SLPI and IFN-g were studied in healthy donors (HDs) and TB patients. Peripheral blood mononuclear cells from HDs and patients with TB or defective IFN-g receptor 1* were stimulated with Mtb antigen and SLPI, and IFN-gR expression levels were measured. Both SLPI and IFN-g were significantly enhanced in plasma from those with TB compared with HDs. A direct association between SLPI levels and the severity of TB was detected. In addition, Mtb antigen stimulation decreased the SLPI produced by peripheral blood mononuclear cells from HDs, but not from TB or IFN-gR patients. Neutralization of IFN-g reversed the inhibition of SLPI induced by Mtb antigen in HDs, but not in TB patients. Furthermore, recombinant IFN-g was unable to modify the expression of SLPI in TB patients. Finally, IFN-gR expression was lower in TB compared with HD peripheral blood mononuclear cells. These results show that Mtb-induced IFN-g down-modulated SLPI levels by signaling through the IFNgR in HDs. This inhibitory mechanism was not observed in TB, probably because of the low expression of IFN-gR detected in these individuals. (Am J Pathol 2014, 184: 1e6
Fil: Tateosian, Nancy Liliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina; Argentina
Fil: Pasquinelli, Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires; Argentina
Fil: Hernández Del Pino, Rodrigo Emanuel. Universidad de Buenos Aires; Argentina
Fil: Ambrosi, Nella Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina; Argentina
Fil: Guerrieri, Diego. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina; Argentina
Fil: Pedraza Sánchez, Sigifredo. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; México
Fil: Santucci, Natalia Estefanía. Universidad Nacional de Rosario; Argentina
Fil: D'attilio, Luciano David. Universidad Nacional de Rosario; Argentina
Fil: Pellegrini, Joaquín Miguel. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Araujo Solis, María A.. Instituto Mexicano del Seguro Social; México
Fil: Musella, Rosa M.. Hospital "F. J. Muñiz"; Argentina
Fil: Palmero, Domingo J.. Hospital "F. J. Muñiz"; Argentina
Fil: Hernandez Pando, Rogelio. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; México
Fil: Garcia, Veronica Edith. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Chuluyan, Hector Eduardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina; Argentina - Materia
-
TUBERCULOSIS
IFN-g
SLPI
RECEPTOR - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/15280
Ver los metadatos del registro completo
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The Impact of IFN-g; Receptor on SLPI Expression in Active Tuberculosis: Association with Disease SeverityTateosian, Nancy LilianaPasquinelli, VirginiaHernández Del Pino, Rodrigo EmanuelAmbrosi, Nella GabrielaGuerrieri, DiegoPedraza Sánchez, SigifredoSantucci, Natalia EstefaníaD'attilio, Luciano DavidPellegrini, Joaquín MiguelAraujo Solis, María A.Musella, Rosa M.Palmero, Domingo J.Hernandez Pando, RogelioGarcia, Veronica EdithChuluyan, Hector EduardoTUBERCULOSISIFN-gSLPIRECEPTORhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Interferon (IFN)-g displays a critical role in tuberculosis (TB), modulating the innate and adaptive immune responses. Previously, we reported that secretory leukocyte protease inhibitor (SLPI) is a pattern recognition receptor with anti-mycobacterial activity against Mycobacterium tuberculosis (Mtb). Herein, we determined whether IFN-g modulated the levels of SLPI in TB patients. Plasma levels of SLPI and IFN-g were studied in healthy donors (HDs) and TB patients. Peripheral blood mononuclear cells from HDs and patients with TB or defective IFN-g receptor 1* were stimulated with Mtb antigen and SLPI, and IFN-gR expression levels were measured. Both SLPI and IFN-g were significantly enhanced in plasma from those with TB compared with HDs. A direct association between SLPI levels and the severity of TB was detected. In addition, Mtb antigen stimulation decreased the SLPI produced by peripheral blood mononuclear cells from HDs, but not from TB or IFN-gR patients. Neutralization of IFN-g reversed the inhibition of SLPI induced by Mtb antigen in HDs, but not in TB patients. Furthermore, recombinant IFN-g was unable to modify the expression of SLPI in TB patients. Finally, IFN-gR expression was lower in TB compared with HD peripheral blood mononuclear cells. These results show that Mtb-induced IFN-g down-modulated SLPI levels by signaling through the IFNgR in HDs. This inhibitory mechanism was not observed in TB, probably because of the low expression of IFN-gR detected in these individuals. (Am J Pathol 2014, 184: 1e6Fil: Tateosian, Nancy Liliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina; ArgentinaFil: Pasquinelli, Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires; ArgentinaFil: Hernández Del Pino, Rodrigo Emanuel. Universidad de Buenos Aires; ArgentinaFil: Ambrosi, Nella Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina; ArgentinaFil: Guerrieri, Diego. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina; ArgentinaFil: Pedraza Sánchez, Sigifredo. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; MéxicoFil: Santucci, Natalia Estefanía. Universidad Nacional de Rosario; ArgentinaFil: D'attilio, Luciano David. Universidad Nacional de Rosario; ArgentinaFil: Pellegrini, Joaquín Miguel. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Araujo Solis, María A.. Instituto Mexicano del Seguro Social; MéxicoFil: Musella, Rosa M.. Hospital "F. J. Muñiz"; ArgentinaFil: Palmero, Domingo J.. Hospital "F. J. Muñiz"; ArgentinaFil: Hernandez Pando, Rogelio. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; MéxicoFil: Garcia, Veronica Edith. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Chuluyan, Hector Eduardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina; ArgentinaAmer Soc Investigative Pathology, Inc2014-05info: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/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/15280Tateosian, Nancy Liliana; Pasquinelli, Virginia; Hernández Del Pino, Rodrigo Emanuel; Ambrosi, Nella Gabriela; Guerrieri, Diego; et al.; The Impact of IFN-g; Receptor on SLPI Expression in Active Tuberculosis: Association with Disease Severity; Amer Soc Investigative Pathology, Inc; American Journal Of Pathology; 184; 5; 5-2014; 1268–12730002-9440enginfo:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0002944014000765info:eu-repo/semantics/altIdentifier/doi/10.1016/j.ajpath.2014.01.006info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:49:00Zoai:ri.conicet.gov.ar:11336/15280instacron: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 09:49:01.249CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
The Impact of IFN-g; Receptor on SLPI Expression in Active Tuberculosis: Association with Disease Severity |
title |
The Impact of IFN-g; Receptor on SLPI Expression in Active Tuberculosis: Association with Disease Severity |
spellingShingle |
The Impact of IFN-g; Receptor on SLPI Expression in Active Tuberculosis: Association with Disease Severity Tateosian, Nancy Liliana TUBERCULOSIS IFN-g SLPI RECEPTOR |
title_short |
The Impact of IFN-g; Receptor on SLPI Expression in Active Tuberculosis: Association with Disease Severity |
title_full |
The Impact of IFN-g; Receptor on SLPI Expression in Active Tuberculosis: Association with Disease Severity |
title_fullStr |
The Impact of IFN-g; Receptor on SLPI Expression in Active Tuberculosis: Association with Disease Severity |
title_full_unstemmed |
The Impact of IFN-g; Receptor on SLPI Expression in Active Tuberculosis: Association with Disease Severity |
title_sort |
The Impact of IFN-g; Receptor on SLPI Expression in Active Tuberculosis: Association with Disease Severity |
dc.creator.none.fl_str_mv |
Tateosian, Nancy Liliana Pasquinelli, Virginia Hernández Del Pino, Rodrigo Emanuel Ambrosi, Nella Gabriela Guerrieri, Diego Pedraza Sánchez, Sigifredo Santucci, Natalia Estefanía D'attilio, Luciano David Pellegrini, Joaquín Miguel Araujo Solis, María A. Musella, Rosa M. Palmero, Domingo J. Hernandez Pando, Rogelio Garcia, Veronica Edith Chuluyan, Hector Eduardo |
author |
Tateosian, Nancy Liliana |
author_facet |
Tateosian, Nancy Liliana Pasquinelli, Virginia Hernández Del Pino, Rodrigo Emanuel Ambrosi, Nella Gabriela Guerrieri, Diego Pedraza Sánchez, Sigifredo Santucci, Natalia Estefanía D'attilio, Luciano David Pellegrini, Joaquín Miguel Araujo Solis, María A. Musella, Rosa M. Palmero, Domingo J. Hernandez Pando, Rogelio Garcia, Veronica Edith Chuluyan, Hector Eduardo |
author_role |
author |
author2 |
Pasquinelli, Virginia Hernández Del Pino, Rodrigo Emanuel Ambrosi, Nella Gabriela Guerrieri, Diego Pedraza Sánchez, Sigifredo Santucci, Natalia Estefanía D'attilio, Luciano David Pellegrini, Joaquín Miguel Araujo Solis, María A. Musella, Rosa M. Palmero, Domingo J. Hernandez Pando, Rogelio Garcia, Veronica Edith Chuluyan, Hector Eduardo |
author2_role |
author author author author author author author author author author author author author author |
dc.subject.none.fl_str_mv |
TUBERCULOSIS IFN-g SLPI RECEPTOR |
topic |
TUBERCULOSIS IFN-g SLPI RECEPTOR |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Interferon (IFN)-g displays a critical role in tuberculosis (TB), modulating the innate and adaptive immune responses. Previously, we reported that secretory leukocyte protease inhibitor (SLPI) is a pattern recognition receptor with anti-mycobacterial activity against Mycobacterium tuberculosis (Mtb). Herein, we determined whether IFN-g modulated the levels of SLPI in TB patients. Plasma levels of SLPI and IFN-g were studied in healthy donors (HDs) and TB patients. Peripheral blood mononuclear cells from HDs and patients with TB or defective IFN-g receptor 1* were stimulated with Mtb antigen and SLPI, and IFN-gR expression levels were measured. Both SLPI and IFN-g were significantly enhanced in plasma from those with TB compared with HDs. A direct association between SLPI levels and the severity of TB was detected. In addition, Mtb antigen stimulation decreased the SLPI produced by peripheral blood mononuclear cells from HDs, but not from TB or IFN-gR patients. Neutralization of IFN-g reversed the inhibition of SLPI induced by Mtb antigen in HDs, but not in TB patients. Furthermore, recombinant IFN-g was unable to modify the expression of SLPI in TB patients. Finally, IFN-gR expression was lower in TB compared with HD peripheral blood mononuclear cells. These results show that Mtb-induced IFN-g down-modulated SLPI levels by signaling through the IFNgR in HDs. This inhibitory mechanism was not observed in TB, probably because of the low expression of IFN-gR detected in these individuals. (Am J Pathol 2014, 184: 1e6 Fil: Tateosian, Nancy Liliana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina; Argentina Fil: Pasquinelli, Virginia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires; Argentina Fil: Hernández Del Pino, Rodrigo Emanuel. Universidad de Buenos Aires; Argentina Fil: Ambrosi, Nella Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina; Argentina Fil: Guerrieri, Diego. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina; Argentina Fil: Pedraza Sánchez, Sigifredo. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; México Fil: Santucci, Natalia Estefanía. Universidad Nacional de Rosario; Argentina Fil: D'attilio, Luciano David. Universidad Nacional de Rosario; Argentina Fil: Pellegrini, Joaquín Miguel. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Araujo Solis, María A.. Instituto Mexicano del Seguro Social; México Fil: Musella, Rosa M.. Hospital "F. J. Muñiz"; Argentina Fil: Palmero, Domingo J.. Hospital "F. J. Muñiz"; Argentina Fil: Hernandez Pando, Rogelio. Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán; México Fil: Garcia, Veronica Edith. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Chuluyan, Hector Eduardo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Estudios Farmacológicos y Botánicos; Argentina; Argentina |
description |
Interferon (IFN)-g displays a critical role in tuberculosis (TB), modulating the innate and adaptive immune responses. Previously, we reported that secretory leukocyte protease inhibitor (SLPI) is a pattern recognition receptor with anti-mycobacterial activity against Mycobacterium tuberculosis (Mtb). Herein, we determined whether IFN-g modulated the levels of SLPI in TB patients. Plasma levels of SLPI and IFN-g were studied in healthy donors (HDs) and TB patients. Peripheral blood mononuclear cells from HDs and patients with TB or defective IFN-g receptor 1* were stimulated with Mtb antigen and SLPI, and IFN-gR expression levels were measured. Both SLPI and IFN-g were significantly enhanced in plasma from those with TB compared with HDs. A direct association between SLPI levels and the severity of TB was detected. In addition, Mtb antigen stimulation decreased the SLPI produced by peripheral blood mononuclear cells from HDs, but not from TB or IFN-gR patients. Neutralization of IFN-g reversed the inhibition of SLPI induced by Mtb antigen in HDs, but not in TB patients. Furthermore, recombinant IFN-g was unable to modify the expression of SLPI in TB patients. Finally, IFN-gR expression was lower in TB compared with HD peripheral blood mononuclear cells. These results show that Mtb-induced IFN-g down-modulated SLPI levels by signaling through the IFNgR in HDs. This inhibitory mechanism was not observed in TB, probably because of the low expression of IFN-gR detected in these individuals. (Am J Pathol 2014, 184: 1e6 |
publishDate |
2014 |
dc.date.none.fl_str_mv |
2014-05 |
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/11336/15280 Tateosian, Nancy Liliana; Pasquinelli, Virginia; Hernández Del Pino, Rodrigo Emanuel; Ambrosi, Nella Gabriela; Guerrieri, Diego; et al.; The Impact of IFN-g; Receptor on SLPI Expression in Active Tuberculosis: Association with Disease Severity; Amer Soc Investigative Pathology, Inc; American Journal Of Pathology; 184; 5; 5-2014; 1268–1273 0002-9440 |
url |
http://hdl.handle.net/11336/15280 |
identifier_str_mv |
Tateosian, Nancy Liliana; Pasquinelli, Virginia; Hernández Del Pino, Rodrigo Emanuel; Ambrosi, Nella Gabriela; Guerrieri, Diego; et al.; The Impact of IFN-g; Receptor on SLPI Expression in Active Tuberculosis: Association with Disease Severity; Amer Soc Investigative Pathology, Inc; American Journal Of Pathology; 184; 5; 5-2014; 1268–1273 0002-9440 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0002944014000765 info:eu-repo/semantics/altIdentifier/doi/10.1016/j.ajpath.2014.01.006 |
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/ |
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application/pdf application/pdf application/pdf application/pdf application/pdf application/pdf application/pdf application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Amer Soc Investigative Pathology, Inc |
publisher.none.fl_str_mv |
Amer Soc Investigative Pathology, Inc |
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reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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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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