Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-beta

Autores
Yaseen, Hiba; Butenko, Sergei; Polishuk Zotkin, Irina; Schif Zuck, Sagie; Pérez Sáez, Juan Manuel; Rabinovich, Gabriel Adrián; Ariel, Amiram
Año de publicación
2020
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
During the resolution of acute inflammation, macrophages undergo reprogramming from pro-inflammatory, to anti-inflammatory/reparative, and eventually to pro-resolving macrophages. Galectin-1 (Gal-1) is a bona fide pro-resolving lectin while interferon β (IFN-β) was recently shown to facilitate macrophage reprogramming and resolution of inflammation. In this study, we found Gal-1null mice exhibit a hyperinflammatory phenotype during the resolution of zymosan A-induced peritonitis but not during the early inflammatory response. This phenotype was characterized by reduced macrophage numbers, increased secretion of pro-inflammatory cytokines, such as interleukin-12 (IL-12), and reduced secretion of anti-inflammatory cytokines, such as interleukin-10 (IL-10). In addition, we found a delayed expression of the pro-resolving enzyme 12/15-lipoxygenase in macrophages and heightened levels of the inflammatory protease proteinase-3 (PR3) in peritoneal fluids from Gal-1null mice. Moreover, we observed sex-dependent differences in the inflammatory profile of Gal-1null mice. Notably, we found that IFN-β levels were reduced in resolution-phase exudates from Gal-1null mice. Administration of IFN-β in vivo or ex vivo treatment was able to rescue, at least in part, the hyperinflammatory profile of Gal-1null mice. In particular, IFN-β recovered a subset of F4/80+GR-1+ macrophages, restored IL-12 and IL-10 secretion from macrophages to WT values and diminished abnormal peritoneal PR3 levels in Gal-1null mice. In conclusion, our results revealed a new Gal-1-IFN-β axis that facilitates the resolution of inflammation and might restrain uncontrolled inflammatory disorders.
Fil: Yaseen, Hiba. University of Haifa; Israel
Fil: Butenko, Sergei. University of Haifa; Israel
Fil: Polishuk Zotkin, Irina. University of Haifa; Israel
Fil: Schif Zuck, Sagie. University of Haifa; Israel
Fil: Pérez Sáez, Juan Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Ariel, Amiram. University of Haifa; Israel
Materia
GALECTIN-1
INTERFERON-Β
MACROPHAGE REPROGRAMMING
PROTEINASE 3
RESOLUTION OF INFLAMMATION
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:11336/142383

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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-betaYaseen, HibaButenko, SergeiPolishuk Zotkin, IrinaSchif Zuck, SagiePérez Sáez, Juan ManuelRabinovich, Gabriel AdriánAriel, AmiramGALECTIN-1INTERFERON-ΒMACROPHAGE REPROGRAMMINGPROTEINASE 3RESOLUTION OF INFLAMMATIONhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3During the resolution of acute inflammation, macrophages undergo reprogramming from pro-inflammatory, to anti-inflammatory/reparative, and eventually to pro-resolving macrophages. Galectin-1 (Gal-1) is a bona fide pro-resolving lectin while interferon β (IFN-β) was recently shown to facilitate macrophage reprogramming and resolution of inflammation. In this study, we found Gal-1null mice exhibit a hyperinflammatory phenotype during the resolution of zymosan A-induced peritonitis but not during the early inflammatory response. This phenotype was characterized by reduced macrophage numbers, increased secretion of pro-inflammatory cytokines, such as interleukin-12 (IL-12), and reduced secretion of anti-inflammatory cytokines, such as interleukin-10 (IL-10). In addition, we found a delayed expression of the pro-resolving enzyme 12/15-lipoxygenase in macrophages and heightened levels of the inflammatory protease proteinase-3 (PR3) in peritoneal fluids from Gal-1null mice. Moreover, we observed sex-dependent differences in the inflammatory profile of Gal-1null mice. Notably, we found that IFN-β levels were reduced in resolution-phase exudates from Gal-1null mice. Administration of IFN-β in vivo or ex vivo treatment was able to rescue, at least in part, the hyperinflammatory profile of Gal-1null mice. In particular, IFN-β recovered a subset of F4/80+GR-1+ macrophages, restored IL-12 and IL-10 secretion from macrophages to WT values and diminished abnormal peritoneal PR3 levels in Gal-1null mice. In conclusion, our results revealed a new Gal-1-IFN-β axis that facilitates the resolution of inflammation and might restrain uncontrolled inflammatory disorders.Fil: Yaseen, Hiba. University of Haifa; IsraelFil: Butenko, Sergei. University of Haifa; IsraelFil: Polishuk Zotkin, Irina. University of Haifa; IsraelFil: Schif Zuck, Sagie. University of Haifa; IsraelFil: Pérez Sáez, Juan Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Ariel, Amiram. University of Haifa; IsraelFrontiers Media S.A.2020-06info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/vnd.openxmlformats-officedocument.wordprocessingml.documentapplication/pdfhttp://hdl.handle.net/11336/142383Yaseen, Hiba; Butenko, Sergei; Polishuk Zotkin, Irina; Schif Zuck, Sagie; Pérez Sáez, Juan Manuel; et al.; Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-beta; Frontiers Media S.A.; Frontiers in Pharmacology; 11; 6-2020; 1-171663-9812CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/journals/pharmacologyinfo:eu-repo/semantics/altIdentifier/doi/10.3389/fphar.2020.00901info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:11:23Zoai:ri.conicet.gov.ar:11336/142383instacron: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 10:11:23.431CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-beta
title Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-beta
spellingShingle Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-beta
Yaseen, Hiba
GALECTIN-1
INTERFERON-Β
MACROPHAGE REPROGRAMMING
PROTEINASE 3
RESOLUTION OF INFLAMMATION
title_short Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-beta
title_full Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-beta
title_fullStr Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-beta
title_full_unstemmed Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-beta
title_sort Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-beta
dc.creator.none.fl_str_mv Yaseen, Hiba
Butenko, Sergei
Polishuk Zotkin, Irina
Schif Zuck, Sagie
Pérez Sáez, Juan Manuel
Rabinovich, Gabriel Adrián
Ariel, Amiram
author Yaseen, Hiba
author_facet Yaseen, Hiba
Butenko, Sergei
Polishuk Zotkin, Irina
Schif Zuck, Sagie
Pérez Sáez, Juan Manuel
Rabinovich, Gabriel Adrián
Ariel, Amiram
author_role author
author2 Butenko, Sergei
Polishuk Zotkin, Irina
Schif Zuck, Sagie
Pérez Sáez, Juan Manuel
Rabinovich, Gabriel Adrián
Ariel, Amiram
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv GALECTIN-1
INTERFERON-Β
MACROPHAGE REPROGRAMMING
PROTEINASE 3
RESOLUTION OF INFLAMMATION
topic GALECTIN-1
INTERFERON-Β
MACROPHAGE REPROGRAMMING
PROTEINASE 3
RESOLUTION OF INFLAMMATION
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv During the resolution of acute inflammation, macrophages undergo reprogramming from pro-inflammatory, to anti-inflammatory/reparative, and eventually to pro-resolving macrophages. Galectin-1 (Gal-1) is a bona fide pro-resolving lectin while interferon β (IFN-β) was recently shown to facilitate macrophage reprogramming and resolution of inflammation. In this study, we found Gal-1null mice exhibit a hyperinflammatory phenotype during the resolution of zymosan A-induced peritonitis but not during the early inflammatory response. This phenotype was characterized by reduced macrophage numbers, increased secretion of pro-inflammatory cytokines, such as interleukin-12 (IL-12), and reduced secretion of anti-inflammatory cytokines, such as interleukin-10 (IL-10). In addition, we found a delayed expression of the pro-resolving enzyme 12/15-lipoxygenase in macrophages and heightened levels of the inflammatory protease proteinase-3 (PR3) in peritoneal fluids from Gal-1null mice. Moreover, we observed sex-dependent differences in the inflammatory profile of Gal-1null mice. Notably, we found that IFN-β levels were reduced in resolution-phase exudates from Gal-1null mice. Administration of IFN-β in vivo or ex vivo treatment was able to rescue, at least in part, the hyperinflammatory profile of Gal-1null mice. In particular, IFN-β recovered a subset of F4/80+GR-1+ macrophages, restored IL-12 and IL-10 secretion from macrophages to WT values and diminished abnormal peritoneal PR3 levels in Gal-1null mice. In conclusion, our results revealed a new Gal-1-IFN-β axis that facilitates the resolution of inflammation and might restrain uncontrolled inflammatory disorders.
Fil: Yaseen, Hiba. University of Haifa; Israel
Fil: Butenko, Sergei. University of Haifa; Israel
Fil: Polishuk Zotkin, Irina. University of Haifa; Israel
Fil: Schif Zuck, Sagie. University of Haifa; Israel
Fil: Pérez Sáez, Juan Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina
Fil: Ariel, Amiram. University of Haifa; Israel
description During the resolution of acute inflammation, macrophages undergo reprogramming from pro-inflammatory, to anti-inflammatory/reparative, and eventually to pro-resolving macrophages. Galectin-1 (Gal-1) is a bona fide pro-resolving lectin while interferon β (IFN-β) was recently shown to facilitate macrophage reprogramming and resolution of inflammation. In this study, we found Gal-1null mice exhibit a hyperinflammatory phenotype during the resolution of zymosan A-induced peritonitis but not during the early inflammatory response. This phenotype was characterized by reduced macrophage numbers, increased secretion of pro-inflammatory cytokines, such as interleukin-12 (IL-12), and reduced secretion of anti-inflammatory cytokines, such as interleukin-10 (IL-10). In addition, we found a delayed expression of the pro-resolving enzyme 12/15-lipoxygenase in macrophages and heightened levels of the inflammatory protease proteinase-3 (PR3) in peritoneal fluids from Gal-1null mice. Moreover, we observed sex-dependent differences in the inflammatory profile of Gal-1null mice. Notably, we found that IFN-β levels were reduced in resolution-phase exudates from Gal-1null mice. Administration of IFN-β in vivo or ex vivo treatment was able to rescue, at least in part, the hyperinflammatory profile of Gal-1null mice. In particular, IFN-β recovered a subset of F4/80+GR-1+ macrophages, restored IL-12 and IL-10 secretion from macrophages to WT values and diminished abnormal peritoneal PR3 levels in Gal-1null mice. In conclusion, our results revealed a new Gal-1-IFN-β axis that facilitates the resolution of inflammation and might restrain uncontrolled inflammatory disorders.
publishDate 2020
dc.date.none.fl_str_mv 2020-06
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/11336/142383
Yaseen, Hiba; Butenko, Sergei; Polishuk Zotkin, Irina; Schif Zuck, Sagie; Pérez Sáez, Juan Manuel; et al.; Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-beta; Frontiers Media S.A.; Frontiers in Pharmacology; 11; 6-2020; 1-17
1663-9812
CONICET Digital
CONICET
url http://hdl.handle.net/11336/142383
identifier_str_mv Yaseen, Hiba; Butenko, Sergei; Polishuk Zotkin, Irina; Schif Zuck, Sagie; Pérez Sáez, Juan Manuel; et al.; Galectin-1 facilitates macrophage reprogramming and resolution of inflammation through IFN-beta; Frontiers Media S.A.; Frontiers in Pharmacology; 11; 6-2020; 1-17
1663-9812
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/journals/pharmacology
info:eu-repo/semantics/altIdentifier/doi/10.3389/fphar.2020.00901
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/vnd.openxmlformats-officedocument.wordprocessingml.document
application/pdf
dc.publisher.none.fl_str_mv Frontiers Media S.A.
publisher.none.fl_str_mv Frontiers Media S.A.
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
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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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