Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarmin

Autores: Russo, Ashley J.; Vasudevan, Swathy O.; Mendez Huergo, Santiago Patricio; Kumari, Puja; Menoret, Antoine; Duduskar, Shivalee; Wang, Chengliang; Pérez Sáez, Juan Manuel; Fettis, Margaret M.; Li, Chuan; Liu, Renjie; Wanchoo, Arun; Chandiran, Karthik; Ruan, Jianbin; Vanaja, Sivapriya Kailasan; Bauer, Michael; Sponholz, Christoph; Hudalla, Gregory A.; Vella, Anthony T.; Zhou, Beiyan; Deshmukh, Sachin D.; Rabinovich, Gabriel Adrián; Rathinam, Vijay A.
Año de publicación: 2021
Idioma: inglés
Tipo de recurso: artículo
Estado: versión publicada
Descripción: Inflammatory caspase sensing of cytosolic lipopolysaccharide (LPS) triggers pyroptosis and the concurrent release of damage-associated molecular patterns (DAMPs). Collectively, DAMPs are key determinants that shape the aftermath of inflammatory cell death. However, the identity and function of the individual DAMPs released are poorly defined. Our proteomics study revealed that cytosolic LPS sensing triggered the release of galectin-1, a β-galactoside-binding lectin. Galectin-1 release is a common feature of inflammatory cell death, including necroptosis. In vivo studies using galectin-1-deficient mice, recombinant galectin-1 and galectin-1-neutralizing antibody showed that galectin-1 promotes inflammation and plays a detrimental role in LPS-induced lethality. Mechanistically, galectin-1 inhibition of CD45 (Ptprc) underlies its unfavorable role in endotoxin shock. Finally, we found increased galectin-1 in sera from human patients with sepsis. Overall, we uncovered galectin-1 as a bona fide DAMP released as a consequence of cytosolic LPS sensing, identifying a new outcome of inflammatory cell death.
Fil: Russo, Ashley J.. UConn Health School of Medicine; Estados Unidos
Fil: Vasudevan, Swathy O.. UConn Health School of Medicine; Estados Unidos
Fil: Mendez Huergo, Santiago Patricio. 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: Kumari, Puja. UConn Health School of Medicine; Estados Unidos
Fil: Menoret, Antoine. UConn Health School of Medicine; Estados Unidos
Fil: Duduskar, Shivalee. Jena University Hospital; Alemania
Fil: Wang, Chengliang. UConn Health School of Medicine; Estados Unidos
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: Fettis, Margaret M.. University of Florida; Estados Unidos
Fil: Li, Chuan. UConn Health School of Medicine; Estados Unidos
Fil: Liu, Renjie. University of Florida; Estados Unidos
Fil: Wanchoo, Arun. University of Florida; Estados Unidos
Fil: Chandiran, Karthik. UConn Health School of Medicine; Estados Unidos
Fil: Ruan, Jianbin. UConn Health School of Medicine; Estados Unidos
Fil: Vanaja, Sivapriya Kailasan. UConn Health School of Medicine; Estados Unidos
Fil: Bauer, Michael. Jena University Hospital; Alemania
Fil: Sponholz, Christoph. Jena University Hospital; Alemania
Fil: Hudalla, Gregory A.. University of Florida; Estados Unidos
Fil: Vella, Anthony T.. UConn Health School of Medicine; Estados Unidos
Fil: Zhou, Beiyan. UConn Health School of Medicine; Estados Unidos
Fil: Deshmukh, Sachin D.. Jena University Hospital; Alemania
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: Rathinam, Vijay A.. UConn Health School of Medicine; Estados Unidos
Materia: GASDERMIN-D
GALECTIN-1
Nivel de accesibilidad: acceso abierto
Condiciones de uso: https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
Institución: Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador: oai:ri.conicet.gov.ar:11336/216594

Acceder

id	CONICETDig_eb07617fb8040da4932f9428a129f230
oai_identifier_str	oai:ri.conicet.gov.ar:11336/216594
network_acronym_str	CONICETDig
repository_id_str	3498
network_name_str	CONICET Digital (CONICET)
spelling	Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarminRusso, Ashley J.Vasudevan, Swathy O.Mendez Huergo, Santiago PatricioKumari, PujaMenoret, AntoineDuduskar, ShivaleeWang, ChengliangPérez Sáez, Juan ManuelFettis, Margaret M.Li, ChuanLiu, RenjieWanchoo, ArunChandiran, KarthikRuan, JianbinVanaja, Sivapriya KailasanBauer, MichaelSponholz, ChristophHudalla, Gregory A.Vella, Anthony T.Zhou, BeiyanDeshmukh, Sachin D.Rabinovich, Gabriel AdriánRathinam, Vijay A.GASDERMIN-DGALECTIN-1https://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Inflammatory caspase sensing of cytosolic lipopolysaccharide (LPS) triggers pyroptosis and the concurrent release of damage-associated molecular patterns (DAMPs). Collectively, DAMPs are key determinants that shape the aftermath of inflammatory cell death. However, the identity and function of the individual DAMPs released are poorly defined. Our proteomics study revealed that cytosolic LPS sensing triggered the release of galectin-1, a β-galactoside-binding lectin. Galectin-1 release is a common feature of inflammatory cell death, including necroptosis. In vivo studies using galectin-1-deficient mice, recombinant galectin-1 and galectin-1-neutralizing antibody showed that galectin-1 promotes inflammation and plays a detrimental role in LPS-induced lethality. Mechanistically, galectin-1 inhibition of CD45 (Ptprc) underlies its unfavorable role in endotoxin shock. Finally, we found increased galectin-1 in sera from human patients with sepsis. Overall, we uncovered galectin-1 as a bona fide DAMP released as a consequence of cytosolic LPS sensing, identifying a new outcome of inflammatory cell death.Fil: Russo, Ashley J.. UConn Health School of Medicine; Estados UnidosFil: Vasudevan, Swathy O.. UConn Health School of Medicine; Estados UnidosFil: Mendez Huergo, Santiago Patricio. 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: Kumari, Puja. UConn Health School of Medicine; Estados UnidosFil: Menoret, Antoine. UConn Health School of Medicine; Estados UnidosFil: Duduskar, Shivalee. Jena University Hospital; AlemaniaFil: Wang, Chengliang. UConn Health School of Medicine; Estados UnidosFil: 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: Fettis, Margaret M.. University of Florida; Estados UnidosFil: Li, Chuan. UConn Health School of Medicine; Estados UnidosFil: Liu, Renjie. University of Florida; Estados UnidosFil: Wanchoo, Arun. University of Florida; Estados UnidosFil: Chandiran, Karthik. UConn Health School of Medicine; Estados UnidosFil: Ruan, Jianbin. UConn Health School of Medicine; Estados UnidosFil: Vanaja, Sivapriya Kailasan. UConn Health School of Medicine; Estados UnidosFil: Bauer, Michael. Jena University Hospital; AlemaniaFil: Sponholz, Christoph. Jena University Hospital; AlemaniaFil: Hudalla, Gregory A.. University of Florida; Estados UnidosFil: Vella, Anthony T.. UConn Health School of Medicine; Estados UnidosFil: Zhou, Beiyan. UConn Health School of Medicine; Estados UnidosFil: Deshmukh, Sachin D.. Jena University Hospital; AlemaniaFil: 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: Rathinam, Vijay A.. UConn Health School of Medicine; Estados UnidosNature Publishing Group2021-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/216594Russo, Ashley J.; Vasudevan, Swathy O.; Mendez Huergo, Santiago Patricio; Kumari, Puja; Menoret, Antoine; et al.; Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarmin; Nature Publishing Group; Nature Immunology (print); 22; 2; 2-2021; 154-1651529-2908CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1038/s41590-020-00844-7info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-11-05T10:50:49Zoai:ri.conicet.gov.ar:11336/216594instacron: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:34982025-11-05 10:50:49.281CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv	Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarmin
title	Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarmin
spellingShingle	Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarmin Russo, Ashley J. GASDERMIN-D GALECTIN-1
title_short	Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarmin
title_full	Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarmin
title_fullStr	Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarmin
title_full_unstemmed	Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarmin
title_sort	Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarmin
dc.creator.none.fl_str_mv	Russo, Ashley J. Vasudevan, Swathy O. Mendez Huergo, Santiago Patricio Kumari, Puja Menoret, Antoine Duduskar, Shivalee Wang, Chengliang Pérez Sáez, Juan Manuel Fettis, Margaret M. Li, Chuan Liu, Renjie Wanchoo, Arun Chandiran, Karthik Ruan, Jianbin Vanaja, Sivapriya Kailasan Bauer, Michael Sponholz, Christoph Hudalla, Gregory A. Vella, Anthony T. Zhou, Beiyan Deshmukh, Sachin D. Rabinovich, Gabriel Adrián Rathinam, Vijay A.
author	Russo, Ashley J.
author_facet	Russo, Ashley J. Vasudevan, Swathy O. Mendez Huergo, Santiago Patricio Kumari, Puja Menoret, Antoine Duduskar, Shivalee Wang, Chengliang Pérez Sáez, Juan Manuel Fettis, Margaret M. Li, Chuan Liu, Renjie Wanchoo, Arun Chandiran, Karthik Ruan, Jianbin Vanaja, Sivapriya Kailasan Bauer, Michael Sponholz, Christoph Hudalla, Gregory A. Vella, Anthony T. Zhou, Beiyan Deshmukh, Sachin D. Rabinovich, Gabriel Adrián Rathinam, Vijay A.
author_role	author
author2	Vasudevan, Swathy O. Mendez Huergo, Santiago Patricio Kumari, Puja Menoret, Antoine Duduskar, Shivalee Wang, Chengliang Pérez Sáez, Juan Manuel Fettis, Margaret M. Li, Chuan Liu, Renjie Wanchoo, Arun Chandiran, Karthik Ruan, Jianbin Vanaja, Sivapriya Kailasan Bauer, Michael Sponholz, Christoph Hudalla, Gregory A. Vella, Anthony T. Zhou, Beiyan Deshmukh, Sachin D. Rabinovich, Gabriel Adrián Rathinam, Vijay A.
author2_role	author author author author author author author author author author author author author author author author author author author author author author
dc.subject.none.fl_str_mv	GASDERMIN-D GALECTIN-1
topic	GASDERMIN-D GALECTIN-1
purl_subject.fl_str_mv	https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv	Inflammatory caspase sensing of cytosolic lipopolysaccharide (LPS) triggers pyroptosis and the concurrent release of damage-associated molecular patterns (DAMPs). Collectively, DAMPs are key determinants that shape the aftermath of inflammatory cell death. However, the identity and function of the individual DAMPs released are poorly defined. Our proteomics study revealed that cytosolic LPS sensing triggered the release of galectin-1, a β-galactoside-binding lectin. Galectin-1 release is a common feature of inflammatory cell death, including necroptosis. In vivo studies using galectin-1-deficient mice, recombinant galectin-1 and galectin-1-neutralizing antibody showed that galectin-1 promotes inflammation and plays a detrimental role in LPS-induced lethality. Mechanistically, galectin-1 inhibition of CD45 (Ptprc) underlies its unfavorable role in endotoxin shock. Finally, we found increased galectin-1 in sera from human patients with sepsis. Overall, we uncovered galectin-1 as a bona fide DAMP released as a consequence of cytosolic LPS sensing, identifying a new outcome of inflammatory cell death. Fil: Russo, Ashley J.. UConn Health School of Medicine; Estados Unidos Fil: Vasudevan, Swathy O.. UConn Health School of Medicine; Estados Unidos Fil: Mendez Huergo, Santiago Patricio. 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: Kumari, Puja. UConn Health School of Medicine; Estados Unidos Fil: Menoret, Antoine. UConn Health School of Medicine; Estados Unidos Fil: Duduskar, Shivalee. Jena University Hospital; Alemania Fil: Wang, Chengliang. UConn Health School of Medicine; Estados Unidos 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: Fettis, Margaret M.. University of Florida; Estados Unidos Fil: Li, Chuan. UConn Health School of Medicine; Estados Unidos Fil: Liu, Renjie. University of Florida; Estados Unidos Fil: Wanchoo, Arun. University of Florida; Estados Unidos Fil: Chandiran, Karthik. UConn Health School of Medicine; Estados Unidos Fil: Ruan, Jianbin. UConn Health School of Medicine; Estados Unidos Fil: Vanaja, Sivapriya Kailasan. UConn Health School of Medicine; Estados Unidos Fil: Bauer, Michael. Jena University Hospital; Alemania Fil: Sponholz, Christoph. Jena University Hospital; Alemania Fil: Hudalla, Gregory A.. University of Florida; Estados Unidos Fil: Vella, Anthony T.. UConn Health School of Medicine; Estados Unidos Fil: Zhou, Beiyan. UConn Health School of Medicine; Estados Unidos Fil: Deshmukh, Sachin D.. Jena University Hospital; Alemania 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: Rathinam, Vijay A.. UConn Health School of Medicine; Estados Unidos
description	Inflammatory caspase sensing of cytosolic lipopolysaccharide (LPS) triggers pyroptosis and the concurrent release of damage-associated molecular patterns (DAMPs). Collectively, DAMPs are key determinants that shape the aftermath of inflammatory cell death. However, the identity and function of the individual DAMPs released are poorly defined. Our proteomics study revealed that cytosolic LPS sensing triggered the release of galectin-1, a β-galactoside-binding lectin. Galectin-1 release is a common feature of inflammatory cell death, including necroptosis. In vivo studies using galectin-1-deficient mice, recombinant galectin-1 and galectin-1-neutralizing antibody showed that galectin-1 promotes inflammation and plays a detrimental role in LPS-induced lethality. Mechanistically, galectin-1 inhibition of CD45 (Ptprc) underlies its unfavorable role in endotoxin shock. Finally, we found increased galectin-1 in sera from human patients with sepsis. Overall, we uncovered galectin-1 as a bona fide DAMP released as a consequence of cytosolic LPS sensing, identifying a new outcome of inflammatory cell death.
publishDate	2021
dc.date.none.fl_str_mv	2021-02
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/11336/216594 Russo, Ashley J.; Vasudevan, Swathy O.; Mendez Huergo, Santiago Patricio; Kumari, Puja; Menoret, Antoine; et al.; Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarmin; Nature Publishing Group; Nature Immunology (print); 22; 2; 2-2021; 154-165 1529-2908 CONICET Digital CONICET
url	http://hdl.handle.net/11336/216594
identifier_str_mv	Russo, Ashley J.; Vasudevan, Swathy O.; Mendez Huergo, Santiago Patricio; Kumari, Puja; Menoret, Antoine; et al.; Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarmin; Nature Publishing Group; Nature Immunology (print); 22; 2; 2-2021; 154-165 1529-2908 CONICET Digital CONICET
dc.language.none.fl_str_mv	eng
language	eng
dc.relation.none.fl_str_mv	info:eu-repo/semantics/altIdentifier/doi/10.1038/s41590-020-00844-7
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
dc.publisher.none.fl_str_mv	Nature Publishing Group
publisher.none.fl_str_mv	Nature Publishing Group
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
_version_	1847978227868368896
score	13.087074

Intracellular immune sensing promotes inflammation via gasdermin D–driven release of a lectin alarmin

Publicaciones similares