Association of haemolytic uraemic syndrome with dysregulation of chemokine receptor expression in circulating monocytes
- Autores
- Ramos, Maria Victoria; Ruggieri, Matias; Panek, Cecilia Analía; Mejias, María Pilar; Fernández Brando, Romina Jimena; Abrey Recalde, Maria Jimena; Exeni, Andrea; Barilari, Catalina; Exeni, Ramon; Palermo, Marina Sandra
- Año de publicación
- 2015
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Haemolytic uraemic syndrome (HUS) is the major complication of Escherichia coli gastrointestinal infections that are Shiga toxin (Stx) producing. Monocytes contribute to HUS evolution by producing cytokines that sensitize endothelial cells to Stx action and migration to the injured kidney. As CC chemokine receptors (CCRs) are involved in monocyte recruitment to injured tissue, we analysed the contribution of these receptors to the pathogenesis of HUS. We analysed CCR1, CCR2 and CCR5 expression in peripheral monocytes from HUS patients during the acute period, with healthy children as controls. We observed an increased expression of CCRs per cell in monocytes from HUS patients, accompanied by an increase in the absolute number of monocytes CCR1+, CCR2+ and CCR5+. It is interesting that prospective analysis confirmed that CCR1 expression positively correlated with HUS severity. The evaluation of chemokine levels in plasma showed that regulated on activation of normal T-cell-expressed and -secreted (RANTES) protein was reduced in plasma from patients with severe HUS, and this decrease correlated with thrombocytopenia. Finally, the expression of the higher CCRs was accompanied by a loss of functionality which could be due to a mechanism for desensitization to compensate for altered receptor expression. The increase in CCR expression correlates with HUS severity, suggesting that the dysregulation of these receptors might contribute to an increased risk of renal damage. Activated monocytes could be recruited by chemokines and then receptors could be dysregulated. The dysregulation of CCRs and their ligands observed during the acute period suggests that a chemokine pathway would participate in HUS development.
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: Ruggieri, Matias. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Panek, Cecilia Analía. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; 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: 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: 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: Exeni, Andrea. Hospital Municipal del Niño; Argentina
Fil: Barilari, Catalina. Municipio de La Matanza. Hospital Municipal del Niño; Argentina
Fil: Exeni, Ramon. Municipio de La Matanza. Hospital Municipal del Niño; 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
-
CHEMOKINE RECEPTORS
FUNCTIONALITY
HUS
MONOCYTES
SHIGA TOXIN
UP-REGULATION - 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:11336/84646
Ver los metadatos del registro completo
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Association of haemolytic uraemic syndrome with dysregulation of chemokine receptor expression in circulating monocytesRamos, Maria VictoriaRuggieri, MatiasPanek, Cecilia AnalíaMejias, María PilarFernández Brando, Romina JimenaAbrey Recalde, Maria JimenaExeni, AndreaBarilari, CatalinaExeni, RamonPalermo, Marina SandraCHEMOKINE RECEPTORSFUNCTIONALITYHUSMONOCYTESSHIGA TOXINUP-REGULATIONhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Haemolytic uraemic syndrome (HUS) is the major complication of Escherichia coli gastrointestinal infections that are Shiga toxin (Stx) producing. Monocytes contribute to HUS evolution by producing cytokines that sensitize endothelial cells to Stx action and migration to the injured kidney. As CC chemokine receptors (CCRs) are involved in monocyte recruitment to injured tissue, we analysed the contribution of these receptors to the pathogenesis of HUS. We analysed CCR1, CCR2 and CCR5 expression in peripheral monocytes from HUS patients during the acute period, with healthy children as controls. We observed an increased expression of CCRs per cell in monocytes from HUS patients, accompanied by an increase in the absolute number of monocytes CCR1+, CCR2+ and CCR5+. It is interesting that prospective analysis confirmed that CCR1 expression positively correlated with HUS severity. The evaluation of chemokine levels in plasma showed that regulated on activation of normal T-cell-expressed and -secreted (RANTES) protein was reduced in plasma from patients with severe HUS, and this decrease correlated with thrombocytopenia. Finally, the expression of the higher CCRs was accompanied by a loss of functionality which could be due to a mechanism for desensitization to compensate for altered receptor expression. The increase in CCR expression correlates with HUS severity, suggesting that the dysregulation of these receptors might contribute to an increased risk of renal damage. Activated monocytes could be recruited by chemokines and then receptors could be dysregulated. The dysregulation of CCRs and their ligands observed during the acute period suggests that a chemokine pathway would participate in HUS development.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; ArgentinaFil: Ruggieri, Matias. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Panek, Cecilia Analía. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; 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: 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: 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: Exeni, Andrea. Hospital Municipal del Niño; ArgentinaFil: Barilari, Catalina. Municipio de La Matanza. Hospital Municipal del Niño; ArgentinaFil: Exeni, Ramon. Municipio de La Matanza. Hospital Municipal del Niño; 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; ArgentinaPortland Press2015-08info: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/11336/84646Ramos, Maria Victoria; Ruggieri, Matias; Panek, Cecilia Analía; Mejias, María Pilar; Fernández Brando, Romina Jimena; et al.; Association of haemolytic uraemic syndrome with dysregulation of chemokine receptor expression in circulating monocytes; Portland Press; Clinical Science; 129; 3; 8-2015; 235-2440143-5221CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.clinsci.org/content/129/3/235.longinfo:eu-repo/semantics/altIdentifier/doi/10.1042/CS20150016info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:27:08Zoai:ri.conicet.gov.ar:11336/84646instacron: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:34982025-09-29 10:27:08.328CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Association of haemolytic uraemic syndrome with dysregulation of chemokine receptor expression in circulating monocytes |
title |
Association of haemolytic uraemic syndrome with dysregulation of chemokine receptor expression in circulating monocytes |
spellingShingle |
Association of haemolytic uraemic syndrome with dysregulation of chemokine receptor expression in circulating monocytes Ramos, Maria Victoria CHEMOKINE RECEPTORS FUNCTIONALITY HUS MONOCYTES SHIGA TOXIN UP-REGULATION |
title_short |
Association of haemolytic uraemic syndrome with dysregulation of chemokine receptor expression in circulating monocytes |
title_full |
Association of haemolytic uraemic syndrome with dysregulation of chemokine receptor expression in circulating monocytes |
title_fullStr |
Association of haemolytic uraemic syndrome with dysregulation of chemokine receptor expression in circulating monocytes |
title_full_unstemmed |
Association of haemolytic uraemic syndrome with dysregulation of chemokine receptor expression in circulating monocytes |
title_sort |
Association of haemolytic uraemic syndrome with dysregulation of chemokine receptor expression in circulating monocytes |
dc.creator.none.fl_str_mv |
Ramos, Maria Victoria Ruggieri, Matias Panek, Cecilia Analía Mejias, María Pilar Fernández Brando, Romina Jimena Abrey Recalde, Maria Jimena Exeni, Andrea Barilari, Catalina Exeni, Ramon Palermo, Marina Sandra |
author |
Ramos, Maria Victoria |
author_facet |
Ramos, Maria Victoria Ruggieri, Matias Panek, Cecilia Analía Mejias, María Pilar Fernández Brando, Romina Jimena Abrey Recalde, Maria Jimena Exeni, Andrea Barilari, Catalina Exeni, Ramon Palermo, Marina Sandra |
author_role |
author |
author2 |
Ruggieri, Matias Panek, Cecilia Analía Mejias, María Pilar Fernández Brando, Romina Jimena Abrey Recalde, Maria Jimena Exeni, Andrea Barilari, Catalina Exeni, Ramon Palermo, Marina Sandra |
author2_role |
author author author author author author author author author |
dc.subject.none.fl_str_mv |
CHEMOKINE RECEPTORS FUNCTIONALITY HUS MONOCYTES SHIGA TOXIN UP-REGULATION |
topic |
CHEMOKINE RECEPTORS FUNCTIONALITY HUS MONOCYTES SHIGA TOXIN UP-REGULATION |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
dc.description.none.fl_txt_mv |
Haemolytic uraemic syndrome (HUS) is the major complication of Escherichia coli gastrointestinal infections that are Shiga toxin (Stx) producing. Monocytes contribute to HUS evolution by producing cytokines that sensitize endothelial cells to Stx action and migration to the injured kidney. As CC chemokine receptors (CCRs) are involved in monocyte recruitment to injured tissue, we analysed the contribution of these receptors to the pathogenesis of HUS. We analysed CCR1, CCR2 and CCR5 expression in peripheral monocytes from HUS patients during the acute period, with healthy children as controls. We observed an increased expression of CCRs per cell in monocytes from HUS patients, accompanied by an increase in the absolute number of monocytes CCR1+, CCR2+ and CCR5+. It is interesting that prospective analysis confirmed that CCR1 expression positively correlated with HUS severity. The evaluation of chemokine levels in plasma showed that regulated on activation of normal T-cell-expressed and -secreted (RANTES) protein was reduced in plasma from patients with severe HUS, and this decrease correlated with thrombocytopenia. Finally, the expression of the higher CCRs was accompanied by a loss of functionality which could be due to a mechanism for desensitization to compensate for altered receptor expression. The increase in CCR expression correlates with HUS severity, suggesting that the dysregulation of these receptors might contribute to an increased risk of renal damage. Activated monocytes could be recruited by chemokines and then receptors could be dysregulated. The dysregulation of CCRs and their ligands observed during the acute period suggests that a chemokine pathway would participate in HUS development. 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: Ruggieri, Matias. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina Fil: Panek, Cecilia Analía. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; 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: 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: 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: Exeni, Andrea. Hospital Municipal del Niño; Argentina Fil: Barilari, Catalina. Municipio de La Matanza. Hospital Municipal del Niño; Argentina Fil: Exeni, Ramon. Municipio de La Matanza. Hospital Municipal del Niño; 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 |
Haemolytic uraemic syndrome (HUS) is the major complication of Escherichia coli gastrointestinal infections that are Shiga toxin (Stx) producing. Monocytes contribute to HUS evolution by producing cytokines that sensitize endothelial cells to Stx action and migration to the injured kidney. As CC chemokine receptors (CCRs) are involved in monocyte recruitment to injured tissue, we analysed the contribution of these receptors to the pathogenesis of HUS. We analysed CCR1, CCR2 and CCR5 expression in peripheral monocytes from HUS patients during the acute period, with healthy children as controls. We observed an increased expression of CCRs per cell in monocytes from HUS patients, accompanied by an increase in the absolute number of monocytes CCR1+, CCR2+ and CCR5+. It is interesting that prospective analysis confirmed that CCR1 expression positively correlated with HUS severity. The evaluation of chemokine levels in plasma showed that regulated on activation of normal T-cell-expressed and -secreted (RANTES) protein was reduced in plasma from patients with severe HUS, and this decrease correlated with thrombocytopenia. Finally, the expression of the higher CCRs was accompanied by a loss of functionality which could be due to a mechanism for desensitization to compensate for altered receptor expression. The increase in CCR expression correlates with HUS severity, suggesting that the dysregulation of these receptors might contribute to an increased risk of renal damage. Activated monocytes could be recruited by chemokines and then receptors could be dysregulated. The dysregulation of CCRs and their ligands observed during the acute period suggests that a chemokine pathway would participate in HUS development. |
publishDate |
2015 |
dc.date.none.fl_str_mv |
2015-08 |
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/11336/84646 Ramos, Maria Victoria; Ruggieri, Matias; Panek, Cecilia Analía; Mejias, María Pilar; Fernández Brando, Romina Jimena; et al.; Association of haemolytic uraemic syndrome with dysregulation of chemokine receptor expression in circulating monocytes; Portland Press; Clinical Science; 129; 3; 8-2015; 235-244 0143-5221 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/84646 |
identifier_str_mv |
Ramos, Maria Victoria; Ruggieri, Matias; Panek, Cecilia Analía; Mejias, María Pilar; Fernández Brando, Romina Jimena; et al.; Association of haemolytic uraemic syndrome with dysregulation of chemokine receptor expression in circulating monocytes; Portland Press; Clinical Science; 129; 3; 8-2015; 235-244 0143-5221 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.clinsci.org/content/129/3/235.long info:eu-repo/semantics/altIdentifier/doi/10.1042/CS20150016 |
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 application/pdf |
dc.publisher.none.fl_str_mv |
Portland Press |
publisher.none.fl_str_mv |
Portland Press |
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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1844614273225981952 |
score |
13.070432 |