Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherich...
- Autores
- Vasconcelos Esteves Pinto, Alipio; Goldstein Raij, Jorge
- Año de publicación
- 2023
- Idioma
- inglés
- Tipo de recurso
- conjunto de datos
- Estado
- Descripción
- Shiga toxin 2 (Stx2) from enterohemorrhagic Escherichia coli (EHEC) produces hemorrhagic colitis, hemolytic uremic syndrome (HUS) and acute encephalopathy. The mortality rate in HUS increases significantly when the central nervous system (CNS) is involved. Besides, EHEC also releases lipopolysaccharide (LPS). Many reports have described cognitive dysfunctions in HUS patients, the hippocampus being one of the brain areas targeted by EHEC infection. In this context, a translational murine model of encephalopathy was employed to establish the deleterious effects of Stx2 and the contribution of LPS in the hippocampus. The purpose of this work is to elucidate the signaling pathways that may activate the inflammatory processes triggered by Stx2, which produces cognitive alterations at the level of the hippocampus. Results demonstrate that Stx2 produced depression-like behavior, pro-inflammatory cytokine release and NF-kB activation independent of the ERK1/2 signaling pathway, while co-administration of Stx2 and LPS reduced memory index. On the other hand, LPS activated NF-kB dependent on ERK1/2 signaling pathway. Cotreatment of Stx2 with LPS aggravated the pathologic state, while dexamethasone treatment succeeded in preventing behavioral alterations. Our present work suggests that the use of drugs such as corticosteroids or NF-kB signaling inhibitors may serve as neuroprotectors from EHEC infection.
Fil: Vasconcelos Esteves Pinto, Alipio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Goldstein Raij, Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina - Nivel de accesibilidad
- acceso restringido
- Condiciones de uso
- Datos sujetos al derecho de propiedad intelectual
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/196042
Ver los metadatos del registro completo
id |
CONICETDig_365ac0955fcba73b68f412b107fad0ff |
---|---|
oai_identifier_str |
oai:ri.conicet.gov.ar:11336/196042 |
network_acronym_str |
CONICETDig |
repository_id_str |
3498 |
network_name_str |
CONICET Digital (CONICET) |
spelling |
Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coliVasconcelos Esteves Pinto, AlipioGoldstein Raij, Jorgehttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Shiga toxin 2 (Stx2) from enterohemorrhagic Escherichia coli (EHEC) produces hemorrhagic colitis, hemolytic uremic syndrome (HUS) and acute encephalopathy. The mortality rate in HUS increases significantly when the central nervous system (CNS) is involved. Besides, EHEC also releases lipopolysaccharide (LPS). Many reports have described cognitive dysfunctions in HUS patients, the hippocampus being one of the brain areas targeted by EHEC infection. In this context, a translational murine model of encephalopathy was employed to establish the deleterious effects of Stx2 and the contribution of LPS in the hippocampus. The purpose of this work is to elucidate the signaling pathways that may activate the inflammatory processes triggered by Stx2, which produces cognitive alterations at the level of the hippocampus. Results demonstrate that Stx2 produced depression-like behavior, pro-inflammatory cytokine release and NF-kB activation independent of the ERK1/2 signaling pathway, while co-administration of Stx2 and LPS reduced memory index. On the other hand, LPS activated NF-kB dependent on ERK1/2 signaling pathway. Cotreatment of Stx2 with LPS aggravated the pathologic state, while dexamethasone treatment succeeded in preventing behavioral alterations. Our present work suggests that the use of drugs such as corticosteroids or NF-kB signaling inhibitors may serve as neuroprotectors from EHEC infection.Fil: Vasconcelos Esteves Pinto, Alipio. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Goldstein Raij, Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina2023info:ar-repo/semantics/conjuntoDeDatosv1.0info:eu-repo/semantics/dataSetapplication/vnd.openxmlformats-officedocument.wordprocessingml.documentimage/tiffapplication/pdfhttp://hdl.handle.net/11336/196042Vasconcelos Esteves Pinto, Alipio; Goldstein Raij, Jorge; (2023): Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coli. Consejo Nacional de Investigaciones Científicas y Técnicas. (dataset). http://hdl.handle.net/11336/196042CONICET DigitalCONICETenginfo:eu-repo/grantAgreement/Ministerio de Ciencia, Tecnología e Innovación Productiva. Agencia Nacional de Promoción Científica y Tecnológica. Fondo para la Investigación Científica y Tecnológica/PICT 2016-1175info:eu-repo/grantAgreement/Universidad de Buenos Aires/PICT 2016-1175info:eu-repo/grantAgreement/Consejo Nacional de Investigaciones Científicas y Técnicas/PICT 2016-1175info:eu-repo/grantAgreement/Consejo Nacional de Investigaciones Científicas y Técnicas/PICT 2016-1175info:eu-repo/grantAgreement//PICT 2016-1175info:eu-repo/semantics/restrictedAccessDatos sujetos al derecho de propiedad intelectualreponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:39:12Zoai:ri.conicet.gov.ar:11336/196042instacron: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 09:39:13.016CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coli |
title |
Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coli |
spellingShingle |
Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coli Vasconcelos Esteves Pinto, Alipio |
title_short |
Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coli |
title_full |
Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coli |
title_fullStr |
Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coli |
title_full_unstemmed |
Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coli |
title_sort |
Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coli |
dc.creator.none.fl_str_mv |
Vasconcelos Esteves Pinto, Alipio Goldstein Raij, Jorge |
author |
Vasconcelos Esteves Pinto, Alipio |
author_facet |
Vasconcelos Esteves Pinto, Alipio Goldstein Raij, Jorge |
author_role |
author |
author2 |
Goldstein Raij, Jorge |
author2_role |
author |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.3 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
Shiga toxin 2 (Stx2) from enterohemorrhagic Escherichia coli (EHEC) produces hemorrhagic colitis, hemolytic uremic syndrome (HUS) and acute encephalopathy. The mortality rate in HUS increases significantly when the central nervous system (CNS) is involved. Besides, EHEC also releases lipopolysaccharide (LPS). Many reports have described cognitive dysfunctions in HUS patients, the hippocampus being one of the brain areas targeted by EHEC infection. In this context, a translational murine model of encephalopathy was employed to establish the deleterious effects of Stx2 and the contribution of LPS in the hippocampus. The purpose of this work is to elucidate the signaling pathways that may activate the inflammatory processes triggered by Stx2, which produces cognitive alterations at the level of the hippocampus. Results demonstrate that Stx2 produced depression-like behavior, pro-inflammatory cytokine release and NF-kB activation independent of the ERK1/2 signaling pathway, while co-administration of Stx2 and LPS reduced memory index. On the other hand, LPS activated NF-kB dependent on ERK1/2 signaling pathway. Cotreatment of Stx2 with LPS aggravated the pathologic state, while dexamethasone treatment succeeded in preventing behavioral alterations. Our present work suggests that the use of drugs such as corticosteroids or NF-kB signaling inhibitors may serve as neuroprotectors from EHEC infection. Fil: Vasconcelos Esteves Pinto, Alipio. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Goldstein Raij, Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina |
description |
Shiga toxin 2 (Stx2) from enterohemorrhagic Escherichia coli (EHEC) produces hemorrhagic colitis, hemolytic uremic syndrome (HUS) and acute encephalopathy. The mortality rate in HUS increases significantly when the central nervous system (CNS) is involved. Besides, EHEC also releases lipopolysaccharide (LPS). Many reports have described cognitive dysfunctions in HUS patients, the hippocampus being one of the brain areas targeted by EHEC infection. In this context, a translational murine model of encephalopathy was employed to establish the deleterious effects of Stx2 and the contribution of LPS in the hippocampus. The purpose of this work is to elucidate the signaling pathways that may activate the inflammatory processes triggered by Stx2, which produces cognitive alterations at the level of the hippocampus. Results demonstrate that Stx2 produced depression-like behavior, pro-inflammatory cytokine release and NF-kB activation independent of the ERK1/2 signaling pathway, while co-administration of Stx2 and LPS reduced memory index. On the other hand, LPS activated NF-kB dependent on ERK1/2 signaling pathway. Cotreatment of Stx2 with LPS aggravated the pathologic state, while dexamethasone treatment succeeded in preventing behavioral alterations. Our present work suggests that the use of drugs such as corticosteroids or NF-kB signaling inhibitors may serve as neuroprotectors from EHEC infection. |
publishDate |
2023 |
dc.date.none.fl_str_mv |
2023 |
dc.type.none.fl_str_mv |
info:ar-repo/semantics/conjuntoDeDatos v1.0 info:eu-repo/semantics/dataSet |
format |
dataSet |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/196042 Vasconcelos Esteves Pinto, Alipio; Goldstein Raij, Jorge; (2023): Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coli. Consejo Nacional de Investigaciones Científicas y Técnicas. (dataset). http://hdl.handle.net/11336/196042 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/196042 |
identifier_str_mv |
Vasconcelos Esteves Pinto, Alipio; Goldstein Raij, Jorge; (2023): Cognitive Deficits Found in a Pro-inflammatory State are Independent of ERK1/2 Signaling in the Murine Brain Hippocampus Treated with Shiga Toxin 2 from Enterohemorrhagic Escherichia coli. Consejo Nacional de Investigaciones Científicas y Técnicas. (dataset). http://hdl.handle.net/11336/196042 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/grantAgreement/Ministerio de Ciencia, Tecnología e Innovación Productiva. Agencia Nacional de Promoción Científica y Tecnológica. Fondo para la Investigación Científica y Tecnológica/PICT 2016-1175 info:eu-repo/grantAgreement/Universidad de Buenos Aires/PICT 2016-1175 info:eu-repo/grantAgreement/Consejo Nacional de Investigaciones Científicas y Técnicas/PICT 2016-1175 info:eu-repo/grantAgreement/Consejo Nacional de Investigaciones Científicas y Técnicas/PICT 2016-1175 info:eu-repo/grantAgreement//PICT 2016-1175 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/restrictedAccess Datos sujetos al derecho de propiedad intelectual |
eu_rights_str_mv |
restrictedAccess |
rights_invalid_str_mv |
Datos sujetos al derecho de propiedad intelectual |
dc.format.none.fl_str_mv |
application/vnd.openxmlformats-officedocument.wordprocessingml.document image/tiff application/pdf |
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 |
_version_ |
1844613239986454528 |
score |
13.070432 |