Junin virus-induced astrocytosis is impaired by iNOS inhibition

Autores
Gomez, Ricardo Martin; Yep, Alejandra; Schattner, Mirta Ana; Berria, Maria Isabel
Año de publicación
2003
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Because Junin virus (JV) experimental encephalitis of mice and rats is characterized by mild histopathological changes that do not seem to justify per se lethality after intracerebral infection, such a murine model seems adequate to investigate the potential role of inducible nitric oxide synthase (iNOS) as a pathogenic factor. Concomitant with a predominant astrocyte reaction, increased immunoperoxidase expression of iNOS, mitochondrial superoxide dismutase (SODm) and glutathione peroxidase (GPX) was disclosed in brain of mice infected with JV strain #44. When specific inhibition of iNOS was achieved by intraperitoneal administration of amino guanidine (AG), significantly greater mortality was observed in treated animals (70% vs. 40%), together with similar infective titers (∼107 PFU/g) but lower astrocytosis, as shown by glial fibrillary acidic (GFAP) labeling. As regards SODm and GPX immunochemical expression in neurons, no differences were found between mice with or without AG treatment. The present results suggest that the apparent protective role of nitric oxide (NO), when synthesized by iNOS, is unrelated to reduced viral replication but rather to enhanced astrocyte activation behaving as a beneficial cell response to virus-induced CNS damage. © 2003 Wiley-Liss, Inc.
Fil: Gomez, Ricardo Martin. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
Fil: Yep, Alejandra. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
Fil: Schattner, Mirta Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Berria, Maria Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
Materia
Gfap
Glutathione Peroxidase
Immunoperoxidase
Nitric Oxide
Superoxide Dismutase
Viral Encephalitis
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:11336/65690
Acceder
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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Junin virus-induced astrocytosis is impaired by iNOS inhibitionGomez, Ricardo MartinYep, AlejandraSchattner, Mirta AnaBerria, Maria IsabelGfapGlutathione PeroxidaseImmunoperoxidaseNitric OxideSuperoxide DismutaseViral Encephalitishttps://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3Because Junin virus (JV) experimental encephalitis of mice and rats is characterized by mild histopathological changes that do not seem to justify per se lethality after intracerebral infection, such a murine model seems adequate to investigate the potential role of inducible nitric oxide synthase (iNOS) as a pathogenic factor. Concomitant with a predominant astrocyte reaction, increased immunoperoxidase expression of iNOS, mitochondrial superoxide dismutase (SODm) and glutathione peroxidase (GPX) was disclosed in brain of mice infected with JV strain #44. When specific inhibition of iNOS was achieved by intraperitoneal administration of amino guanidine (AG), significantly greater mortality was observed in treated animals (70% vs. 40%), together with similar infective titers (∼107 PFU/g) but lower astrocytosis, as shown by glial fibrillary acidic (GFAP) labeling. As regards SODm and GPX immunochemical expression in neurons, no differences were found between mice with or without AG treatment. The present results suggest that the apparent protective role of nitric oxide (NO), when synthesized by iNOS, is unrelated to reduced viral replication but rather to enhanced astrocyte activation behaving as a beneficial cell response to virus-induced CNS damage. © 2003 Wiley-Liss, Inc.Fil: Gomez, Ricardo Martin. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; ArgentinaFil: Yep, Alejandra. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; ArgentinaFil: Schattner, Mirta Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Berria, Maria Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; ArgentinaWiley-liss, Div John Wiley & Sons Inc2003-01-20info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/65690Gomez, Ricardo Martin; Yep, Alejandra; Schattner, Mirta Ana; Berria, Maria Isabel; Junin virus-induced astrocytosis is impaired by iNOS inhibition; Wiley-liss, Div John Wiley & Sons Inc; Journal of Medical Virology; 69; 1; 20-1-2003; 145-1490146-6615CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1002/jmv.10254info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1002/jmv.10254info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:41:54Zoai:ri.conicet.gov.ar:11336/65690instacron: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:34982025-10-15 15:41:54.736CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Junin virus-induced astrocytosis is impaired by iNOS inhibition
title Junin virus-induced astrocytosis is impaired by iNOS inhibition
spellingShingle Junin virus-induced astrocytosis is impaired by iNOS inhibition
Gomez, Ricardo Martin
Gfap
Glutathione Peroxidase
Immunoperoxidase
Nitric Oxide
Superoxide Dismutase
Viral Encephalitis
title_short Junin virus-induced astrocytosis is impaired by iNOS inhibition
title_full Junin virus-induced astrocytosis is impaired by iNOS inhibition
title_fullStr Junin virus-induced astrocytosis is impaired by iNOS inhibition
title_full_unstemmed Junin virus-induced astrocytosis is impaired by iNOS inhibition
title_sort Junin virus-induced astrocytosis is impaired by iNOS inhibition
dc.creator.none.fl_str_mv Gomez, Ricardo Martin
Yep, Alejandra
Schattner, Mirta Ana
Berria, Maria Isabel
author Gomez, Ricardo Martin
author_facet Gomez, Ricardo Martin
Yep, Alejandra
Schattner, Mirta Ana
Berria, Maria Isabel
author_role author
author2 Yep, Alejandra
Schattner, Mirta Ana
Berria, Maria Isabel
author2_role author
author
author
dc.subject.none.fl_str_mv Gfap
Glutathione Peroxidase
Immunoperoxidase
Nitric Oxide
Superoxide Dismutase
Viral Encephalitis
topic Gfap
Glutathione Peroxidase
Immunoperoxidase
Nitric Oxide
Superoxide Dismutase
Viral Encephalitis
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Because Junin virus (JV) experimental encephalitis of mice and rats is characterized by mild histopathological changes that do not seem to justify per se lethality after intracerebral infection, such a murine model seems adequate to investigate the potential role of inducible nitric oxide synthase (iNOS) as a pathogenic factor. Concomitant with a predominant astrocyte reaction, increased immunoperoxidase expression of iNOS, mitochondrial superoxide dismutase (SODm) and glutathione peroxidase (GPX) was disclosed in brain of mice infected with JV strain #44. When specific inhibition of iNOS was achieved by intraperitoneal administration of amino guanidine (AG), significantly greater mortality was observed in treated animals (70% vs. 40%), together with similar infective titers (∼107 PFU/g) but lower astrocytosis, as shown by glial fibrillary acidic (GFAP) labeling. As regards SODm and GPX immunochemical expression in neurons, no differences were found between mice with or without AG treatment. The present results suggest that the apparent protective role of nitric oxide (NO), when synthesized by iNOS, is unrelated to reduced viral replication but rather to enhanced astrocyte activation behaving as a beneficial cell response to virus-induced CNS damage. © 2003 Wiley-Liss, Inc.
Fil: Gomez, Ricardo Martin. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
Fil: Yep, Alejandra. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
Fil: Schattner, Mirta Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; Argentina
Fil: Berria, Maria Isabel. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Microbiología; Argentina
description Because Junin virus (JV) experimental encephalitis of mice and rats is characterized by mild histopathological changes that do not seem to justify per se lethality after intracerebral infection, such a murine model seems adequate to investigate the potential role of inducible nitric oxide synthase (iNOS) as a pathogenic factor. Concomitant with a predominant astrocyte reaction, increased immunoperoxidase expression of iNOS, mitochondrial superoxide dismutase (SODm) and glutathione peroxidase (GPX) was disclosed in brain of mice infected with JV strain #44. When specific inhibition of iNOS was achieved by intraperitoneal administration of amino guanidine (AG), significantly greater mortality was observed in treated animals (70% vs. 40%), together with similar infective titers (∼107 PFU/g) but lower astrocytosis, as shown by glial fibrillary acidic (GFAP) labeling. As regards SODm and GPX immunochemical expression in neurons, no differences were found between mice with or without AG treatment. The present results suggest that the apparent protective role of nitric oxide (NO), when synthesized by iNOS, is unrelated to reduced viral replication but rather to enhanced astrocyte activation behaving as a beneficial cell response to virus-induced CNS damage. © 2003 Wiley-Liss, Inc.
publishDate 2003
dc.date.none.fl_str_mv 2003-01-20
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/11336/65690
Gomez, Ricardo Martin; Yep, Alejandra; Schattner, Mirta Ana; Berria, Maria Isabel; Junin virus-induced astrocytosis is impaired by iNOS inhibition; Wiley-liss, Div John Wiley & Sons Inc; Journal of Medical Virology; 69; 1; 20-1-2003; 145-149
0146-6615
CONICET Digital
CONICET
url http://hdl.handle.net/11336/65690
identifier_str_mv Gomez, Ricardo Martin; Yep, Alejandra; Schattner, Mirta Ana; Berria, Maria Isabel; Junin virus-induced astrocytosis is impaired by iNOS inhibition; Wiley-liss, Div John Wiley & Sons Inc; Journal of Medical Virology; 69; 1; 20-1-2003; 145-149
0146-6615
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1002/jmv.10254
info:eu-repo/semantics/altIdentifier/url/https://onlinelibrary.wiley.com/doi/abs/10.1002/jmv.10254
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
dc.publisher.none.fl_str_mv Wiley-liss, Div John Wiley & Sons Inc
publisher.none.fl_str_mv Wiley-liss, Div John Wiley & Sons Inc
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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