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dc.contributor.author
Abrey Recalde, Maria Jimena
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Alvarez, Romina Soledad
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Alberto, Maria Fabiana
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Mejias, María Pilar
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Ramos, Maria Victoria
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Fernández Brando, Romina Jimena
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Bruballa, Andrea Cecilia
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Exeni, Ramon A.
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Alconcher, Laura
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Ibarra, Cristina Adriana
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Amaral, María Marta
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Palermo, Marina Sandra
dc.date.available
2018-04-19T19:59:34Z
dc.date.issued
2017-10-25
dc.identifier.citation
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
dc.identifier.issn
2072-6651
dc.identifier.uri
http://hdl.handle.net/11336/42741
dc.description.abstract
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.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
MDPI AG
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Blood Platelets
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Cd40l
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Hemolytic Uremic Syndrome
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Oxidative Stress
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Shiga Toxin 2
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Enfermedades Infecciosas
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Ciencias de la Salud
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.subject.classification
Enfermedades Infecciosas
dc.subject.classification
Ciencias de la Salud
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Soluble CD40 ligand and oxidative response are reciprocally stimulated during shiga toxin-associated hemolytic uremic syndrome
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-04-09T15:08:47Z
dc.identifier.eissn
2072-6651
dc.journal.volume
9
dc.journal.number
11
dc.journal.pagination
331-331
dc.journal.pais
Suiza
dc.journal.ciudad
Basel
dc.description.fil
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
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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
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Fil: Alberto, Maria Fabiana. Academia Nacional de Medicina de Buenos Aires. Instituto de Investigaciones Hematológicas ; Argentina
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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
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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
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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
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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
dc.description.fil
Fil: Exeni, Ramon A.. Hospital Municipal del Niño de San Justo; Argentina
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Fil: Alconcher, Laura. Provincia de Buenos Aires. Hospital Interzonal General Dr. José Penna; Argentina
dc.description.fil
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
dc.description.fil
Fil: Amaral, María Marta. Universidad de Buenos Aires; Argentina. Universidad de Buenos Aires; Argentina
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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
dc.journal.title
Toxins
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.mdpi.com/2072-6651/9/11/331
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.3390/toxins9110331
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/pmid/29068360
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5705951/
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