Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndrome

Autores
Abrey Recalde, Maria Jimena; Alvarez, Romina Soledad; Alberto, Maria Fabiana; Mejias, María Pilar; Ramos, Maria Victoria; Fernández Brando, Romina Jimena; Bruballa, Andrea Cecilia; Exeni, Ramon A.; Alconcher, Laura; Ibarra, Cristina Adriana; Amaral, María Marta; Palermo, Marina Sandra
Año de publicación
2017
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Shiga toxin (Stx), produced by Escherichia coli, is the main pathogenic factor of diarrhea-associated hemolytic uremic syndrome (HUS), which is characterized by the obstruction of renal microvasculature by platelet-fibrin thrombi. It is well known that the oxidative imbalance generated by Stx induces platelet activation, contributing to thrombus formation. Moreover, activated platelets release soluble CD40 ligand (sCD40L), which in turn contributes to oxidative imbalance, triggering the release of reactive oxidative species (ROS) on various cellular types. The aim of this work was to determine if the interaction between the oxidative response and platelet-derived sCD40L, as consequence of Stx-induced endothelium damage, participates in the pathogenic mechanism during HUS. Activated human glomerular endothelial cells (HGEC) by Stx2 induced platelets to adhere to them. Although platelet adhesion did not contribute to endothelial damage, high levels of sCD40L were released to the medium. The release of sCD40L by activated platelets was inhibited by antioxidant treatment. Furthermore, we found increased levels of sCD40L in plasma from HUS patients, which were also able to trigger the respiratory burst in monocytes in a sCD40L-dependent manner. Thus, we concluded that platelet-derived sCD40L and the oxidative response are reciprocally stimulated during Stx2-associated HUS. This process may contribute to the evolution of glomerular occlusion and the microangiopathic lesions.
Fil: Abrey Recalde, Maria Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Alvarez, Romina Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Alberto, Maria Fabiana. Academia Nacional de Medicina de Buenos Aires. Instituto de Investigaciones Hematológicas ; Argentina
Fil: Mejias, María Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Ramos, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Fernández Brando, Romina Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Bruballa, Andrea Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Exeni, Ramon A.. Hospital Municipal del Niño de San Justo; Argentina
Fil: Alconcher, Laura. Provincia de Buenos Aires. Hospital Interzonal General Dr. José Penna; Argentina
Fil: Ibarra, Cristina Adriana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Amaral, María Marta. Universidad de Buenos Aires; Argentina. Universidad de Buenos Aires; Argentina
Fil: Palermo, Marina Sandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Materia
Blood Platelets
Cd40l
Hemolytic Uremic Syndrome
Oxidative Stress
Shiga Toxin 2
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:11336/42741
Acceder
id CONICETDig_55292ee61bb7da74eee05feb4c205963
oai_identifier_str oai:ri.conicet.gov.ar:11336/42741
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndromeAbrey Recalde, Maria JimenaAlvarez, Romina SoledadAlberto, Maria FabianaMejias, María PilarRamos, Maria VictoriaFernández Brando, Romina JimenaBruballa, Andrea CeciliaExeni, Ramon A.Alconcher, LauraIbarra, Cristina AdrianaAmaral, María MartaPalermo, Marina SandraBlood PlateletsCd40lHemolytic Uremic SyndromeOxidative StressShiga Toxin 2https://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3https://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Shiga toxin (Stx), produced by Escherichia coli, is the main pathogenic factor of diarrhea-associated hemolytic uremic syndrome (HUS), which is characterized by the obstruction of renal microvasculature by platelet-fibrin thrombi. It is well known that the oxidative imbalance generated by Stx induces platelet activation, contributing to thrombus formation. Moreover, activated platelets release soluble CD40 ligand (sCD40L), which in turn contributes to oxidative imbalance, triggering the release of reactive oxidative species (ROS) on various cellular types. The aim of this work was to determine if the interaction between the oxidative response and platelet-derived sCD40L, as consequence of Stx-induced endothelium damage, participates in the pathogenic mechanism during HUS. Activated human glomerular endothelial cells (HGEC) by Stx2 induced platelets to adhere to them. Although platelet adhesion did not contribute to endothelial damage, high levels of sCD40L were released to the medium. The release of sCD40L by activated platelets was inhibited by antioxidant treatment. Furthermore, we found increased levels of sCD40L in plasma from HUS patients, which were also able to trigger the respiratory burst in monocytes in a sCD40L-dependent manner. Thus, we concluded that platelet-derived sCD40L and the oxidative response are reciprocally stimulated during Stx2-associated HUS. This process may contribute to the evolution of glomerular occlusion and the microangiopathic lesions.Fil: Abrey Recalde, Maria Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Alvarez, Romina Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; ArgentinaFil: Alberto, Maria Fabiana. Academia Nacional de Medicina de Buenos Aires. Instituto de Investigaciones Hematológicas ; ArgentinaFil: Mejias, María Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Ramos, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Fernández Brando, Romina Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Bruballa, Andrea Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Exeni, Ramon A.. Hospital Municipal del Niño de San Justo; ArgentinaFil: Alconcher, Laura. Provincia de Buenos Aires. Hospital Interzonal General Dr. José Penna; ArgentinaFil: Ibarra, Cristina Adriana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; ArgentinaFil: Amaral, María Marta. Universidad de Buenos Aires; Argentina. Universidad de Buenos Aires; ArgentinaFil: Palermo, Marina Sandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaMDPI AG2017-10-25info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/42741Abrey Recalde, Maria Jimena; Alvarez, Romina Soledad; Alberto, Maria Fabiana; Mejias, María Pilar; Ramos, Maria Victoria; et al.; Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndrome; MDPI AG; Toxins; 9; 11; 25-10-2017; 331-3312072-66512072-6651CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.mdpi.com/2072-6651/9/11/331info:eu-repo/semantics/altIdentifier/doi/10.3390/toxins9110331info:eu-repo/semantics/altIdentifier/pmid/29068360info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5705951/info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:06:50Zoai:ri.conicet.gov.ar:11336/42741instacron: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 10:06:50.725CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndrome
title Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndrome
spellingShingle Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndrome
Abrey Recalde, Maria Jimena
Blood Platelets
Cd40l
Hemolytic Uremic Syndrome
Oxidative Stress
Shiga Toxin 2
title_short Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndrome
title_full Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndrome
title_fullStr Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndrome
title_full_unstemmed Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndrome
title_sort Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndrome
dc.creator.none.fl_str_mv Abrey Recalde, Maria Jimena
Alvarez, Romina Soledad
Alberto, Maria Fabiana
Mejias, María Pilar
Ramos, Maria Victoria
Fernández Brando, Romina Jimena
Bruballa, Andrea Cecilia
Exeni, Ramon A.
Alconcher, Laura
Ibarra, Cristina Adriana
Amaral, María Marta
Palermo, Marina Sandra
author Abrey Recalde, Maria Jimena
author_facet Abrey Recalde, Maria Jimena
Alvarez, Romina Soledad
Alberto, Maria Fabiana
Mejias, María Pilar
Ramos, Maria Victoria
Fernández Brando, Romina Jimena
Bruballa, Andrea Cecilia
Exeni, Ramon A.
Alconcher, Laura
Ibarra, Cristina Adriana
Amaral, María Marta
Palermo, Marina Sandra
author_role author
author2 Alvarez, Romina Soledad
Alberto, Maria Fabiana
Mejias, María Pilar
Ramos, Maria Victoria
Fernández Brando, Romina Jimena
Bruballa, Andrea Cecilia
Exeni, Ramon A.
Alconcher, Laura
Ibarra, Cristina Adriana
Amaral, María Marta
Palermo, Marina Sandra
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Blood Platelets
Cd40l
Hemolytic Uremic Syndrome
Oxidative Stress
Shiga Toxin 2
topic Blood Platelets
Cd40l
Hemolytic Uremic Syndrome
Oxidative Stress
Shiga Toxin 2
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Shiga toxin (Stx), produced by Escherichia coli, is the main pathogenic factor of diarrhea-associated hemolytic uremic syndrome (HUS), which is characterized by the obstruction of renal microvasculature by platelet-fibrin thrombi. It is well known that the oxidative imbalance generated by Stx induces platelet activation, contributing to thrombus formation. Moreover, activated platelets release soluble CD40 ligand (sCD40L), which in turn contributes to oxidative imbalance, triggering the release of reactive oxidative species (ROS) on various cellular types. The aim of this work was to determine if the interaction between the oxidative response and platelet-derived sCD40L, as consequence of Stx-induced endothelium damage, participates in the pathogenic mechanism during HUS. Activated human glomerular endothelial cells (HGEC) by Stx2 induced platelets to adhere to them. Although platelet adhesion did not contribute to endothelial damage, high levels of sCD40L were released to the medium. The release of sCD40L by activated platelets was inhibited by antioxidant treatment. Furthermore, we found increased levels of sCD40L in plasma from HUS patients, which were also able to trigger the respiratory burst in monocytes in a sCD40L-dependent manner. Thus, we concluded that platelet-derived sCD40L and the oxidative response are reciprocally stimulated during Stx2-associated HUS. This process may contribute to the evolution of glomerular occlusion and the microangiopathic lesions.
Fil: Abrey Recalde, Maria Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Alvarez, Romina Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Alberto, Maria Fabiana. Academia Nacional de Medicina de Buenos Aires. Instituto de Investigaciones Hematológicas ; Argentina
Fil: Mejias, María Pilar. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Ramos, Maria Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Fernández Brando, Romina Jimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Bruballa, Andrea Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Exeni, Ramon A.. Hospital Municipal del Niño de San Justo; Argentina
Fil: Alconcher, Laura. Provincia de Buenos Aires. Hospital Interzonal General Dr. José Penna; Argentina
Fil: Ibarra, Cristina Adriana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
Fil: Amaral, María Marta. Universidad de Buenos Aires; Argentina. Universidad de Buenos Aires; Argentina
Fil: Palermo, Marina Sandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
description Shiga toxin (Stx), produced by Escherichia coli, is the main pathogenic factor of diarrhea-associated hemolytic uremic syndrome (HUS), which is characterized by the obstruction of renal microvasculature by platelet-fibrin thrombi. It is well known that the oxidative imbalance generated by Stx induces platelet activation, contributing to thrombus formation. Moreover, activated platelets release soluble CD40 ligand (sCD40L), which in turn contributes to oxidative imbalance, triggering the release of reactive oxidative species (ROS) on various cellular types. The aim of this work was to determine if the interaction between the oxidative response and platelet-derived sCD40L, as consequence of Stx-induced endothelium damage, participates in the pathogenic mechanism during HUS. Activated human glomerular endothelial cells (HGEC) by Stx2 induced platelets to adhere to them. Although platelet adhesion did not contribute to endothelial damage, high levels of sCD40L were released to the medium. The release of sCD40L by activated platelets was inhibited by antioxidant treatment. Furthermore, we found increased levels of sCD40L in plasma from HUS patients, which were also able to trigger the respiratory burst in monocytes in a sCD40L-dependent manner. Thus, we concluded that platelet-derived sCD40L and the oxidative response are reciprocally stimulated during Stx2-associated HUS. This process may contribute to the evolution of glomerular occlusion and the microangiopathic lesions.
publishDate 2017
dc.date.none.fl_str_mv 2017-10-25
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/11336/42741
Abrey Recalde, Maria Jimena; Alvarez, Romina Soledad; Alberto, Maria Fabiana; Mejias, María Pilar; Ramos, Maria Victoria; et al.; Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndrome; MDPI AG; Toxins; 9; 11; 25-10-2017; 331-331
2072-6651
2072-6651
CONICET Digital
CONICET
url http://hdl.handle.net/11336/42741
identifier_str_mv Abrey Recalde, Maria Jimena; Alvarez, Romina Soledad; Alberto, Maria Fabiana; Mejias, María Pilar; Ramos, Maria Victoria; et al.; Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndrome; MDPI AG; Toxins; 9; 11; 25-10-2017; 331-331
2072-6651
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.mdpi.com/2072-6651/9/11/331
info:eu-repo/semantics/altIdentifier/doi/10.3390/toxins9110331
info:eu-repo/semantics/altIdentifier/pmid/29068360
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5705951/
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
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dc.publisher.none.fl_str_mv MDPI AG
publisher.none.fl_str_mv MDPI AG
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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