Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS)

Autores
Exeni, Ramon Alfonso; Fernández Brando, Romina Jimena; Santiago, Adriana Patricia; Fiorentino, Gabriela Alejandra; Exeni, Andrea Mariana; Ramos, Maria Victoria; Palermo, Marina Sandra
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Hemolytic uremic syndrome (HUS) is defined as a triad of noninmune microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. The most frequent presentation is secondary to Shiga toxin (Stx)-producing Escherichia coli (STEC) infections, which is termed postdiarrheal, epidemiologic or Stx-HUS, considering that Stx is the necessary etiological factor. After ingestion, STEC colonize the intestine and produce Stx, which translocates across the intestinal epithelium. Once Stx enters the bloodstream, it interacts with renal endothelial and epithelial cells, and leukocytes. This review summarizes the current evidence about the involvement of inflammatory components as central pathogenic factors that could determine outcome of STEC infections. Intestinal inflammation may favor epithelial leakage and subsequent passage of Stx to the systemic circulation. Vascular damage triggered by Stx promotes not only release of thrombin and increased fibrin concentration but also production of cytokines and chemokines by endothelial cells. Recent evidence from animal models and patients strongly indicate that several immune cells types may participate in HUS physiopathology: neutrophils, through release of proteases and reactive oxygen species (ROS); monocytes/macrophages through secretion of cytokines and chemokines. In addition, high levels of Bb factor and soluble C5b-9 (sC5b-9) in plasma as well as complement factors adhered to platelet-leukocyte complexes, microparticles and microvesicles, suggest activation of the alternative pathway of complement. Thus, acute immune response secondary to STEC infection, the Stx stimulatory effect on different immune cells, and inflammatory stimulus secondary to endothelial damage all together converge to define a strong inflammatory status that worsens Stx toxicity and disease.
Fil: Exeni, Ramon Alfonso. Provincia de Buenos Aires. Hospital Municipal del Niño; 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: Santiago, Adriana Patricia. Provincia de Buenos Aires. Hospital Municipal del Niño; Argentina
Fil: Fiorentino, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina. Provincia de Buenos Aires. Hospital Municipal del Niño; Argentina
Fil: Exeni, Andrea Mariana. Provincia de Buenos Aires. Hospital Austral; 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: 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
COMPLEMENT
HUS
INFLAMMATION
LEUKOCYTES
SHIGA TOXIN
THROMBOSIS
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:11336/93929
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/93929
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS)Exeni, Ramon AlfonsoFernández Brando, Romina JimenaSantiago, Adriana PatriciaFiorentino, Gabriela AlejandraExeni, Andrea MarianaRamos, Maria VictoriaPalermo, Marina SandraCOMPLEMENTHUSINFLAMMATIONLEUKOCYTESSHIGA TOXINTHROMBOSIShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Hemolytic uremic syndrome (HUS) is defined as a triad of noninmune microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. The most frequent presentation is secondary to Shiga toxin (Stx)-producing Escherichia coli (STEC) infections, which is termed postdiarrheal, epidemiologic or Stx-HUS, considering that Stx is the necessary etiological factor. After ingestion, STEC colonize the intestine and produce Stx, which translocates across the intestinal epithelium. Once Stx enters the bloodstream, it interacts with renal endothelial and epithelial cells, and leukocytes. This review summarizes the current evidence about the involvement of inflammatory components as central pathogenic factors that could determine outcome of STEC infections. Intestinal inflammation may favor epithelial leakage and subsequent passage of Stx to the systemic circulation. Vascular damage triggered by Stx promotes not only release of thrombin and increased fibrin concentration but also production of cytokines and chemokines by endothelial cells. Recent evidence from animal models and patients strongly indicate that several immune cells types may participate in HUS physiopathology: neutrophils, through release of proteases and reactive oxygen species (ROS); monocytes/macrophages through secretion of cytokines and chemokines. In addition, high levels of Bb factor and soluble C5b-9 (sC5b-9) in plasma as well as complement factors adhered to platelet-leukocyte complexes, microparticles and microvesicles, suggest activation of the alternative pathway of complement. Thus, acute immune response secondary to STEC infection, the Stx stimulatory effect on different immune cells, and inflammatory stimulus secondary to endothelial damage all together converge to define a strong inflammatory status that worsens Stx toxicity and disease.Fil: Exeni, Ramon Alfonso. Provincia de Buenos Aires. Hospital Municipal del Niño; 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: Santiago, Adriana Patricia. Provincia de Buenos Aires. Hospital Municipal del Niño; ArgentinaFil: Fiorentino, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina. Provincia de Buenos Aires. Hospital Municipal del Niño; ArgentinaFil: Exeni, Andrea Mariana. Provincia de Buenos Aires. Hospital Austral; 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: 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; ArgentinaSpringer2018-11info: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/11336/93929Exeni, Ramon Alfonso; Fernández Brando, Romina Jimena; Santiago, Adriana Patricia; Fiorentino, Gabriela Alejandra; Exeni, Andrea Mariana; et al.; Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS); Springer; Pediatric Nephrology; 33; 11; 11-2018; 2057-20710931-041XCONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://link.springer.com/10.1007/s00467-017-3876-0info:eu-repo/semantics/altIdentifier/doi/10.1007/s00467-017-3876-0info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:35:26Zoai:ri.conicet.gov.ar:11336/93929instacron: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 09:35:27.17CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS)
title Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS)
spellingShingle Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS)
Exeni, Ramon Alfonso
COMPLEMENT
HUS
INFLAMMATION
LEUKOCYTES
SHIGA TOXIN
THROMBOSIS
title_short Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS)
title_full Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS)
title_fullStr Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS)
title_full_unstemmed Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS)
title_sort Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS)
dc.creator.none.fl_str_mv Exeni, Ramon Alfonso
Fernández Brando, Romina Jimena
Santiago, Adriana Patricia
Fiorentino, Gabriela Alejandra
Exeni, Andrea Mariana
Ramos, Maria Victoria
Palermo, Marina Sandra
author Exeni, Ramon Alfonso
author_facet Exeni, Ramon Alfonso
Fernández Brando, Romina Jimena
Santiago, Adriana Patricia
Fiorentino, Gabriela Alejandra
Exeni, Andrea Mariana
Ramos, Maria Victoria
Palermo, Marina Sandra
author_role author
author2 Fernández Brando, Romina Jimena
Santiago, Adriana Patricia
Fiorentino, Gabriela Alejandra
Exeni, Andrea Mariana
Ramos, Maria Victoria
Palermo, Marina Sandra
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv COMPLEMENT
HUS
INFLAMMATION
LEUKOCYTES
SHIGA TOXIN
THROMBOSIS
topic COMPLEMENT
HUS
INFLAMMATION
LEUKOCYTES
SHIGA TOXIN
THROMBOSIS
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Hemolytic uremic syndrome (HUS) is defined as a triad of noninmune microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. The most frequent presentation is secondary to Shiga toxin (Stx)-producing Escherichia coli (STEC) infections, which is termed postdiarrheal, epidemiologic or Stx-HUS, considering that Stx is the necessary etiological factor. After ingestion, STEC colonize the intestine and produce Stx, which translocates across the intestinal epithelium. Once Stx enters the bloodstream, it interacts with renal endothelial and epithelial cells, and leukocytes. This review summarizes the current evidence about the involvement of inflammatory components as central pathogenic factors that could determine outcome of STEC infections. Intestinal inflammation may favor epithelial leakage and subsequent passage of Stx to the systemic circulation. Vascular damage triggered by Stx promotes not only release of thrombin and increased fibrin concentration but also production of cytokines and chemokines by endothelial cells. Recent evidence from animal models and patients strongly indicate that several immune cells types may participate in HUS physiopathology: neutrophils, through release of proteases and reactive oxygen species (ROS); monocytes/macrophages through secretion of cytokines and chemokines. In addition, high levels of Bb factor and soluble C5b-9 (sC5b-9) in plasma as well as complement factors adhered to platelet-leukocyte complexes, microparticles and microvesicles, suggest activation of the alternative pathway of complement. Thus, acute immune response secondary to STEC infection, the Stx stimulatory effect on different immune cells, and inflammatory stimulus secondary to endothelial damage all together converge to define a strong inflammatory status that worsens Stx toxicity and disease.
Fil: Exeni, Ramon Alfonso. Provincia de Buenos Aires. Hospital Municipal del Niño; 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: Santiago, Adriana Patricia. Provincia de Buenos Aires. Hospital Municipal del Niño; Argentina
Fil: Fiorentino, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina. Provincia de Buenos Aires. Hospital Municipal del Niño; Argentina
Fil: Exeni, Andrea Mariana. Provincia de Buenos Aires. Hospital Austral; 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: 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 Hemolytic uremic syndrome (HUS) is defined as a triad of noninmune microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. The most frequent presentation is secondary to Shiga toxin (Stx)-producing Escherichia coli (STEC) infections, which is termed postdiarrheal, epidemiologic or Stx-HUS, considering that Stx is the necessary etiological factor. After ingestion, STEC colonize the intestine and produce Stx, which translocates across the intestinal epithelium. Once Stx enters the bloodstream, it interacts with renal endothelial and epithelial cells, and leukocytes. This review summarizes the current evidence about the involvement of inflammatory components as central pathogenic factors that could determine outcome of STEC infections. Intestinal inflammation may favor epithelial leakage and subsequent passage of Stx to the systemic circulation. Vascular damage triggered by Stx promotes not only release of thrombin and increased fibrin concentration but also production of cytokines and chemokines by endothelial cells. Recent evidence from animal models and patients strongly indicate that several immune cells types may participate in HUS physiopathology: neutrophils, through release of proteases and reactive oxygen species (ROS); monocytes/macrophages through secretion of cytokines and chemokines. In addition, high levels of Bb factor and soluble C5b-9 (sC5b-9) in plasma as well as complement factors adhered to platelet-leukocyte complexes, microparticles and microvesicles, suggest activation of the alternative pathway of complement. Thus, acute immune response secondary to STEC infection, the Stx stimulatory effect on different immune cells, and inflammatory stimulus secondary to endothelial damage all together converge to define a strong inflammatory status that worsens Stx toxicity and disease.
publishDate 2018
dc.date.none.fl_str_mv 2018-11
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/11336/93929
Exeni, Ramon Alfonso; Fernández Brando, Romina Jimena; Santiago, Adriana Patricia; Fiorentino, Gabriela Alejandra; Exeni, Andrea Mariana; et al.; Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS); Springer; Pediatric Nephrology; 33; 11; 11-2018; 2057-2071
0931-041X
CONICET Digital
CONICET
url http://hdl.handle.net/11336/93929
identifier_str_mv Exeni, Ramon Alfonso; Fernández Brando, Romina Jimena; Santiago, Adriana Patricia; Fiorentino, Gabriela Alejandra; Exeni, Andrea Mariana; et al.; Pathogenic role of inflammatory response during Shiga toxin-associated hemolytic uremic syndrome (HUS); Springer; Pediatric Nephrology; 33; 11; 11-2018; 2057-2071
0931-041X
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://link.springer.com/10.1007/s00467-017-3876-0
info:eu-repo/semantics/altIdentifier/doi/10.1007/s00467-017-3876-0
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 Springer
publisher.none.fl_str_mv Springer
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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score 13.070432

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