Relevance of bacteriophage 933W in the development of hemolytic uremic syndrome (HUS)

Autores
del Cogliano, Manuel Eugenio; Vasconcelos Esteves Pinto, Alipio; Goldstein Raij, Jorge; Zotta, Elsa; Ochoa, Federico Claudio; Fernández Brando, Romina Jimena; Muniesa, Maite; Ghiringhelli, Pablo Daniel; Palermo, Marina Sandra; Bentancor, Leticia Verónica
Año de publicación
2018
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Hemolytic uremic syndrome (HUS), principally caused by Shiga toxins (Stxs), is associated with Shiga toxin-producing Escherichia coli (STEC) infections. We previously reported Stx2 expression by host cells in vitro and in vivo. As the genes encoding the two Stx subunits are located in bacteriophage genomes, the aim of the current study was to evaluate the role of bacteriophage induction in HUS development in absence of an E. coli O157:H7 genomic background. Mice were inoculated with a non-pathogenic E. coli strain carrying the lysogenic bacteriophage 933W (C600Φ933W), and bacteriophage excision was induced by an antibiotic. The mice died 72 h after inoculation, having developed pathogenic damage typical of STEC infection. As well as renal and intestinal damage, markers of central nervous system (CNS) injury were observed, including aberrant immunolocalization of neuronal nuclei (NeuN) and increased expression of glial fibrillary acidic protein (GFAP). These results show that bacteriophage 933W without an E. coli O157:H7 background is capable of inducing the pathogenic damage associated with STEC infection. In addition, a novel mouse model was developed to evaluate therapeutic approaches focused on the bacteriophage as a new target.
Fil: del Cogliano, Manuel Eugenio. Universidad Nacional de Quilmes; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Vasconcelos Esteves Pinto, Alipio. 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: Goldstein Raij, Jorge. 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: Zotta, Elsa. 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: Ochoa, Federico Claudio. 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: 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: Muniesa, Maite. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Ghiringhelli, Pablo Daniel. Universidad Nacional de Quilmes; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; 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
Fil: Bentancor, Leticia Verónica. Universidad Nacional de Quilmes; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Materia
ANIMAL MODEL
BACTERIO(PHAGES)
HEMOLYTIC UREMIC SYNDROME
SHIGA TOXIGENIC E. COLI (STEC)
SHIGA TOXIN (STX)
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/87762
Acceder
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repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Relevance of bacteriophage 933W in the development of hemolytic uremic syndrome (HUS)del Cogliano, Manuel EugenioVasconcelos Esteves Pinto, AlipioGoldstein Raij, JorgeZotta, ElsaOchoa, Federico ClaudioFernández Brando, Romina JimenaMuniesa, MaiteGhiringhelli, Pablo DanielPalermo, Marina SandraBentancor, Leticia VerónicaANIMAL MODELBACTERIO(PHAGES)HEMOLYTIC UREMIC SYNDROMESHIGA TOXIGENIC E. COLI (STEC)SHIGA TOXIN (STX)https://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Hemolytic uremic syndrome (HUS), principally caused by Shiga toxins (Stxs), is associated with Shiga toxin-producing Escherichia coli (STEC) infections. We previously reported Stx2 expression by host cells in vitro and in vivo. As the genes encoding the two Stx subunits are located in bacteriophage genomes, the aim of the current study was to evaluate the role of bacteriophage induction in HUS development in absence of an E. coli O157:H7 genomic background. Mice were inoculated with a non-pathogenic E. coli strain carrying the lysogenic bacteriophage 933W (C600Φ933W), and bacteriophage excision was induced by an antibiotic. The mice died 72 h after inoculation, having developed pathogenic damage typical of STEC infection. As well as renal and intestinal damage, markers of central nervous system (CNS) injury were observed, including aberrant immunolocalization of neuronal nuclei (NeuN) and increased expression of glial fibrillary acidic protein (GFAP). These results show that bacteriophage 933W without an E. coli O157:H7 background is capable of inducing the pathogenic damage associated with STEC infection. In addition, a novel mouse model was developed to evaluate therapeutic approaches focused on the bacteriophage as a new target.Fil: del Cogliano, Manuel Eugenio. Universidad Nacional de Quilmes; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Vasconcelos Esteves Pinto, Alipio. 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: Goldstein Raij, Jorge. 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: Zotta, Elsa. 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: Ochoa, Federico Claudio. 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: 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: Muniesa, Maite. Academia Nacional de Medicina de Buenos Aires; ArgentinaFil: Ghiringhelli, Pablo Daniel. Universidad Nacional de Quilmes; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; 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; ArgentinaFil: Bentancor, Leticia Verónica. Universidad Nacional de Quilmes; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFrontiers Research Foundation2018-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/87762del Cogliano, Manuel Eugenio; Vasconcelos Esteves Pinto, Alipio; Goldstein Raij, Jorge; Zotta, Elsa; Ochoa, Federico Claudio; et al.; Relevance of bacteriophage 933W in the development of hemolytic uremic syndrome (HUS); Frontiers Research Foundation; Frontiers in Microbiology; 9; 3104; 12-2018; 1-111664-302XCONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/article/10.3389/fmicb.2018.03104/fullinfo:eu-repo/semantics/altIdentifier/doi/10.3389/fmicb.2018.03104info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:00:41Zoai:ri.conicet.gov.ar:11336/87762instacron: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 10:00:42.228CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Relevance of bacteriophage 933W in the development of hemolytic uremic syndrome (HUS)
title Relevance of bacteriophage 933W in the development of hemolytic uremic syndrome (HUS)
spellingShingle Relevance of bacteriophage 933W in the development of hemolytic uremic syndrome (HUS)
del Cogliano, Manuel Eugenio
ANIMAL MODEL
BACTERIO(PHAGES)
HEMOLYTIC UREMIC SYNDROME
SHIGA TOXIGENIC E. COLI (STEC)
SHIGA TOXIN (STX)
title_short Relevance of bacteriophage 933W in the development of hemolytic uremic syndrome (HUS)
title_full Relevance of bacteriophage 933W in the development of hemolytic uremic syndrome (HUS)
title_fullStr Relevance of bacteriophage 933W in the development of hemolytic uremic syndrome (HUS)
title_full_unstemmed Relevance of bacteriophage 933W in the development of hemolytic uremic syndrome (HUS)
title_sort Relevance of bacteriophage 933W in the development of hemolytic uremic syndrome (HUS)
dc.creator.none.fl_str_mv del Cogliano, Manuel Eugenio
Vasconcelos Esteves Pinto, Alipio
Goldstein Raij, Jorge
Zotta, Elsa
Ochoa, Federico Claudio
Fernández Brando, Romina Jimena
Muniesa, Maite
Ghiringhelli, Pablo Daniel
Palermo, Marina Sandra
Bentancor, Leticia Verónica
author del Cogliano, Manuel Eugenio
author_facet del Cogliano, Manuel Eugenio
Vasconcelos Esteves Pinto, Alipio
Goldstein Raij, Jorge
Zotta, Elsa
Ochoa, Federico Claudio
Fernández Brando, Romina Jimena
Muniesa, Maite
Ghiringhelli, Pablo Daniel
Palermo, Marina Sandra
Bentancor, Leticia Verónica
author_role author
author2 Vasconcelos Esteves Pinto, Alipio
Goldstein Raij, Jorge
Zotta, Elsa
Ochoa, Federico Claudio
Fernández Brando, Romina Jimena
Muniesa, Maite
Ghiringhelli, Pablo Daniel
Palermo, Marina Sandra
Bentancor, Leticia Verónica
author2_role author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv ANIMAL MODEL
BACTERIO(PHAGES)
HEMOLYTIC UREMIC SYNDROME
SHIGA TOXIGENIC E. COLI (STEC)
SHIGA TOXIN (STX)
topic ANIMAL MODEL
BACTERIO(PHAGES)
HEMOLYTIC UREMIC SYNDROME
SHIGA TOXIGENIC E. COLI (STEC)
SHIGA TOXIN (STX)
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), principally caused by Shiga toxins (Stxs), is associated with Shiga toxin-producing Escherichia coli (STEC) infections. We previously reported Stx2 expression by host cells in vitro and in vivo. As the genes encoding the two Stx subunits are located in bacteriophage genomes, the aim of the current study was to evaluate the role of bacteriophage induction in HUS development in absence of an E. coli O157:H7 genomic background. Mice were inoculated with a non-pathogenic E. coli strain carrying the lysogenic bacteriophage 933W (C600Φ933W), and bacteriophage excision was induced by an antibiotic. The mice died 72 h after inoculation, having developed pathogenic damage typical of STEC infection. As well as renal and intestinal damage, markers of central nervous system (CNS) injury were observed, including aberrant immunolocalization of neuronal nuclei (NeuN) and increased expression of glial fibrillary acidic protein (GFAP). These results show that bacteriophage 933W without an E. coli O157:H7 background is capable of inducing the pathogenic damage associated with STEC infection. In addition, a novel mouse model was developed to evaluate therapeutic approaches focused on the bacteriophage as a new target.
Fil: del Cogliano, Manuel Eugenio. Universidad Nacional de Quilmes; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Vasconcelos Esteves Pinto, Alipio. 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: Goldstein Raij, Jorge. 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: Zotta, Elsa. 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: Ochoa, Federico Claudio. 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: 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: Muniesa, Maite. Academia Nacional de Medicina de Buenos Aires; Argentina
Fil: Ghiringhelli, Pablo Daniel. Universidad Nacional de Quilmes; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; 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
Fil: Bentancor, Leticia Verónica. Universidad Nacional de Quilmes; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
description Hemolytic uremic syndrome (HUS), principally caused by Shiga toxins (Stxs), is associated with Shiga toxin-producing Escherichia coli (STEC) infections. We previously reported Stx2 expression by host cells in vitro and in vivo. As the genes encoding the two Stx subunits are located in bacteriophage genomes, the aim of the current study was to evaluate the role of bacteriophage induction in HUS development in absence of an E. coli O157:H7 genomic background. Mice were inoculated with a non-pathogenic E. coli strain carrying the lysogenic bacteriophage 933W (C600Φ933W), and bacteriophage excision was induced by an antibiotic. The mice died 72 h after inoculation, having developed pathogenic damage typical of STEC infection. As well as renal and intestinal damage, markers of central nervous system (CNS) injury were observed, including aberrant immunolocalization of neuronal nuclei (NeuN) and increased expression of glial fibrillary acidic protein (GFAP). These results show that bacteriophage 933W without an E. coli O157:H7 background is capable of inducing the pathogenic damage associated with STEC infection. In addition, a novel mouse model was developed to evaluate therapeutic approaches focused on the bacteriophage as a new target.
publishDate 2018
dc.date.none.fl_str_mv 2018-12
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/11336/87762
del Cogliano, Manuel Eugenio; Vasconcelos Esteves Pinto, Alipio; Goldstein Raij, Jorge; Zotta, Elsa; Ochoa, Federico Claudio; et al.; Relevance of bacteriophage 933W in the development of hemolytic uremic syndrome (HUS); Frontiers Research Foundation; Frontiers in Microbiology; 9; 3104; 12-2018; 1-11
1664-302X
CONICET Digital
CONICET
url http://hdl.handle.net/11336/87762
identifier_str_mv del Cogliano, Manuel Eugenio; Vasconcelos Esteves Pinto, Alipio; Goldstein Raij, Jorge; Zotta, Elsa; Ochoa, Federico Claudio; et al.; Relevance of bacteriophage 933W in the development of hemolytic uremic syndrome (HUS); Frontiers Research Foundation; Frontiers in Microbiology; 9; 3104; 12-2018; 1-11
1664-302X
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/article/10.3389/fmicb.2018.03104/full
info:eu-repo/semantics/altIdentifier/doi/10.3389/fmicb.2018.03104
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
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dc.publisher.none.fl_str_mv Frontiers Research Foundation
publisher.none.fl_str_mv Frontiers Research Foundation
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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