Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis
Autor(a) principal: | |
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Data de Publicação: | 2017 |
Outros Autores: | , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Arquivos de neuro-psiquiatria (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-282X2017000200005 |
Resumo: | ABSTRACT Neurocysticercosis (NCC) is the most severe clinical manifestation of cysticercosis. One of the factors responsible for its symptomatology is the host inflammatory response. Therefore the influence of interleukin 4 (IL-4) on the induction of encephalitis in experimental NCC was evaluated. Methods BALB/c (WT) and BALB/c (IL-4-KO) mice were inoculated intracranially with Taenia crassiceps cysticerci and euthanized at 7, 30, 60 and 90 days later, the encephala removed and histopathologically analyzed. Results The absence of IL-4 induced greater parasitism. In the initial phase of the infection, IL-4-KO showed a lower intensity in the inflammatory infiltration of polimorphonuclear cells in the host-parasite interface and intra-parenquimatous edema. The IL-4-KO animals, in the late phase of the infection, showed lower intensity of ventriculomegaly, encephalitis, and meningitis, and greater survival of the parasites in comparison with the WT animals. Conclusion The absence of IL-4 induced lower inflammatory infiltration, ventriculomegaly and perivasculitis in experimental NCC. |
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Arquivos de neuro-psiquiatria (Online) |
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Experimental neurocysticercosis: absence of IL-4 induces lower encephalitisneurocysticercosisTaenia crassicepsencephalitisinterleukin-4ABSTRACT Neurocysticercosis (NCC) is the most severe clinical manifestation of cysticercosis. One of the factors responsible for its symptomatology is the host inflammatory response. Therefore the influence of interleukin 4 (IL-4) on the induction of encephalitis in experimental NCC was evaluated. Methods BALB/c (WT) and BALB/c (IL-4-KO) mice were inoculated intracranially with Taenia crassiceps cysticerci and euthanized at 7, 30, 60 and 90 days later, the encephala removed and histopathologically analyzed. Results The absence of IL-4 induced greater parasitism. In the initial phase of the infection, IL-4-KO showed a lower intensity in the inflammatory infiltration of polimorphonuclear cells in the host-parasite interface and intra-parenquimatous edema. The IL-4-KO animals, in the late phase of the infection, showed lower intensity of ventriculomegaly, encephalitis, and meningitis, and greater survival of the parasites in comparison with the WT animals. Conclusion The absence of IL-4 induced lower inflammatory infiltration, ventriculomegaly and perivasculitis in experimental NCC.Academia Brasileira de Neurologia - ABNEURO2017-02-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-282X2017000200005Arquivos de Neuro-Psiquiatria v.75 n.2 2017reponame:Arquivos de neuro-psiquiatria (Online)instname:Academia Brasileira de Neurologiainstacron:ABNEURO10.1590/0004-282x20160194info:eu-repo/semantics/openAccessSilva,Hidelberto MatosVinaud,Marina ClareLino Júnior,Ruy de Souzaeng2017-02-17T00:00:00Zoai:scielo:S0004-282X2017000200005Revistahttp://www.scielo.br/anphttps://old.scielo.br/oai/scielo-oai.php||revista.arquivos@abneuro.org1678-42270004-282Xopendoar:2017-02-17T00:00Arquivos de neuro-psiquiatria (Online) - Academia Brasileira de Neurologiafalse |
dc.title.none.fl_str_mv |
Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis |
title |
Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis |
spellingShingle |
Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis Silva,Hidelberto Matos neurocysticercosis Taenia crassiceps encephalitis interleukin-4 |
title_short |
Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis |
title_full |
Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis |
title_fullStr |
Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis |
title_full_unstemmed |
Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis |
title_sort |
Experimental neurocysticercosis: absence of IL-4 induces lower encephalitis |
author |
Silva,Hidelberto Matos |
author_facet |
Silva,Hidelberto Matos Vinaud,Marina Clare Lino Júnior,Ruy de Souza |
author_role |
author |
author2 |
Vinaud,Marina Clare Lino Júnior,Ruy de Souza |
author2_role |
author author |
dc.contributor.author.fl_str_mv |
Silva,Hidelberto Matos Vinaud,Marina Clare Lino Júnior,Ruy de Souza |
dc.subject.por.fl_str_mv |
neurocysticercosis Taenia crassiceps encephalitis interleukin-4 |
topic |
neurocysticercosis Taenia crassiceps encephalitis interleukin-4 |
description |
ABSTRACT Neurocysticercosis (NCC) is the most severe clinical manifestation of cysticercosis. One of the factors responsible for its symptomatology is the host inflammatory response. Therefore the influence of interleukin 4 (IL-4) on the induction of encephalitis in experimental NCC was evaluated. Methods BALB/c (WT) and BALB/c (IL-4-KO) mice were inoculated intracranially with Taenia crassiceps cysticerci and euthanized at 7, 30, 60 and 90 days later, the encephala removed and histopathologically analyzed. Results The absence of IL-4 induced greater parasitism. In the initial phase of the infection, IL-4-KO showed a lower intensity in the inflammatory infiltration of polimorphonuclear cells in the host-parasite interface and intra-parenquimatous edema. The IL-4-KO animals, in the late phase of the infection, showed lower intensity of ventriculomegaly, encephalitis, and meningitis, and greater survival of the parasites in comparison with the WT animals. Conclusion The absence of IL-4 induced lower inflammatory infiltration, ventriculomegaly and perivasculitis in experimental NCC. |
publishDate |
2017 |
dc.date.none.fl_str_mv |
2017-02-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-282X2017000200005 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-282X2017000200005 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/0004-282x20160194 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Academia Brasileira de Neurologia - ABNEURO |
publisher.none.fl_str_mv |
Academia Brasileira de Neurologia - ABNEURO |
dc.source.none.fl_str_mv |
Arquivos de Neuro-Psiquiatria v.75 n.2 2017 reponame:Arquivos de neuro-psiquiatria (Online) instname:Academia Brasileira de Neurologia instacron:ABNEURO |
instname_str |
Academia Brasileira de Neurologia |
instacron_str |
ABNEURO |
institution |
ABNEURO |
reponame_str |
Arquivos de neuro-psiquiatria (Online) |
collection |
Arquivos de neuro-psiquiatria (Online) |
repository.name.fl_str_mv |
Arquivos de neuro-psiquiatria (Online) - Academia Brasileira de Neurologia |
repository.mail.fl_str_mv |
||revista.arquivos@abneuro.org |
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1754212781785088000 |