Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia

Detalhes bibliográficos
Autor(a) principal: Zolini, Guilherme Pimenta
Data de Publicação: 2014
Outros Autores: Lima, Graciela Kunrath, Lucinda, Natália, Silva, Mariana Almeida, Dias, Marcela França, Pessoa, Natália Lima, Coura, Bruna Pizziolo, Cartelle, Christiane Teixeira, Arantes, Rosa Maria Esteves, Kroon, Erna Geessien, Campos, Marco Antônio
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da FIOCRUZ (ARCA)
Texto Completo: https://www.arca.fiocruz.br/handle/icict/9450
Resumo: Fundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Imunopatologia. Imunologia de Doenças Virais. Belo Horizonte, MG, Brazil.
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spelling Zolini, Guilherme PimentaLima, Graciela KunrathLucinda, NatáliaSilva, Mariana AlmeidaDias, Marcela FrançaPessoa, Natália LimaCoura, Bruna PizzioloCartelle, Christiane TeixeiraArantes, Rosa Maria EstevesKroon, Erna GeessienCampos, Marco Antônio2015-02-06T16:16:35Z2015-02-06T16:16:35Z2014ZOLINI, Guilherme Pimenta et al. Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia. Zolini et al. Journal of Neuroinflammation, v.11, p. 20, 2014.1742-2094https://www.arca.fiocruz.br/handle/icict/945010.1186/1742-2094-11-20engBiomed CentralDefense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal gangliainfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleFundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Imunopatologia. Imunologia de Doenças Virais. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Escola de Veterinária. Belo Horizonte, MG, Brazil.Fundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Imunopatologia. Imunologia de Doenças Virais. Belo Horizonte, MG, Brazil.Fundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Imunopatologia. Imunologia de Doenças Virais. Belo Horizonte, MG, Brazil.Fundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Imunopatologia. Imunologia de Doenças Virais. Belo Horizonte, MG, Brazil.Fundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Imunopatologia. Imunologia de Doenças Virais. Belo Horizonte, MG, Brazil.Fundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Imunopatologia. Imunologia de Doenças Virais. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Departamento de Patologia. Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Departamento de Patologia.Belo Horizonte, MG, Brazil.Universidade Federal de Minas Gerais. Departamento de Microbiologia. Belo Horizonte, MG, Brazil.Fundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Imunopatologia. Imunologia de Doenças Virais. Belo Horizonte, MG, Brazil.Background: Herpes simplex 1 (HSV-1) causes various human clinical manifestations, ranging from simple cold sores to encephalitis. Innate immune cells recognize pathogens through Toll-like receptors (TLRs), thus initiating the immune response. Previously, we demonstrated that the immune response against HSV-1 is dependent on TLR2 and TLR9 expression and on IFN gamma production in the trigeminal ganglia (TG) of infected mice. In this work, we further investigated the cells, molecules, and mechanisms of HSV-1 infection control, especially those that are TLR-dependent. Methods: C57BL/6 wild-type (WT), TLR2−/−, TLR9−/−, and TLR2/9−/− mice were intranasally infected with HSV-1. On the viral peak day, the TG and brains were collected from mice and TLR expression was measured in the TG and brain and inducible nitric oxide synthase (iNOS) expression was measured in the TG by real-time PCR. Immunofluorescence assays were performed in mice TG to detect iNOS production by F4/80+ cells. Intraperitoneal macrophages nitric oxide (NO) production was evaluated by the Griess assay. WT, CD8−/−, RAG−/−, and iNOS−/− mice were intranasally infected in a survival assay, and their cytokine expression was measured in the TG by real-time PCR. Results: Infected WT mice exhibited significantly increased TLR expression, compared with their respective controls, in the TG but not in the brain. TLR-deficient mice had moderately increased TLR expression in the TG and brain in compare with the non-infected animals. iNOS expression in the WT infected mice TG was higher than in the other groups with increased production by macrophages in the WT infected mice, which did not occur in the TLR2/9−/− mice. Additionally, the intraperitoneal macrophages of the WT mice had a higher production of NO compared with those of the TLR-deficient mice. The CD8−/−, RAG−/−, and iNOS−/− mice had 100% mortality after the HSV-1 infection compared with 10% of the WT mice. Cytokines were overexpressed in the iNOS−/− infected mice, while the RAG−/− mice were nearly unresponsive to the virus. Conclusion: TLRs efficiently orchestrate the innate immune cells, eliciting macrophage response (with NO production by the macrophages), thereby controlling the HSV-1 infection through the immune response in the TG of mice.EncephalitisHSV-1Innate immunityToll-like receptorsHost immune responseinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da FIOCRUZ (ARCA)instname:Fundação Oswaldo Cruz (FIOCRUZ)instacron:FIOCRUZLICENSElicense.txtlicense.txttext/plain; charset=utf-81914https://www.arca.fiocruz.br/bitstream/icict/9450/1/license.txt7d48279ffeed55da8dfe2f8e81f3b81fMD51ORIGINAL2014_052.pdf2014_052.pdfapplication/pdf3419407https://www.arca.fiocruz.br/bitstream/icict/9450/2/2014_052.pdf17390aa93f87a1188815245fd73800d4MD52TEXT2014_052.pdf.txt2014_052.pdf.txtExtracted texttext/plain51756https://www.arca.fiocruz.br/bitstream/icict/9450/3/2014_052.pdf.txtbcf9ddbf04ed1d8ab236387b5611c16aMD53icict/94502019-06-19 10:12:08.608oai:www.arca.fiocruz.br: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ório InstitucionalPUBhttps://www.arca.fiocruz.br/oai/requestrepositorio.arca@fiocruz.bropendoar:21352019-06-19T13:12:08Repositório Institucional da FIOCRUZ (ARCA) - Fundação Oswaldo Cruz (FIOCRUZ)false
dc.title.pt_BR.fl_str_mv Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia
title Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia
spellingShingle Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia
Zolini, Guilherme Pimenta
Encephalitis
HSV-1
Innate immunity
Toll-like receptors
Host immune response
title_short Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia
title_full Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia
title_fullStr Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia
title_full_unstemmed Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia
title_sort Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia
author Zolini, Guilherme Pimenta
author_facet Zolini, Guilherme Pimenta
Lima, Graciela Kunrath
Lucinda, Natália
Silva, Mariana Almeida
Dias, Marcela França
Pessoa, Natália Lima
Coura, Bruna Pizziolo
Cartelle, Christiane Teixeira
Arantes, Rosa Maria Esteves
Kroon, Erna Geessien
Campos, Marco Antônio
author_role author
author2 Lima, Graciela Kunrath
Lucinda, Natália
Silva, Mariana Almeida
Dias, Marcela França
Pessoa, Natália Lima
Coura, Bruna Pizziolo
Cartelle, Christiane Teixeira
Arantes, Rosa Maria Esteves
Kroon, Erna Geessien
Campos, Marco Antônio
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Zolini, Guilherme Pimenta
Lima, Graciela Kunrath
Lucinda, Natália
Silva, Mariana Almeida
Dias, Marcela França
Pessoa, Natália Lima
Coura, Bruna Pizziolo
Cartelle, Christiane Teixeira
Arantes, Rosa Maria Esteves
Kroon, Erna Geessien
Campos, Marco Antônio
dc.subject.en.pt_BR.fl_str_mv Encephalitis
HSV-1
Innate immunity
Toll-like receptors
Host immune response
topic Encephalitis
HSV-1
Innate immunity
Toll-like receptors
Host immune response
description Fundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Imunopatologia. Imunologia de Doenças Virais. Belo Horizonte, MG, Brazil.
publishDate 2014
dc.date.issued.fl_str_mv 2014
dc.date.accessioned.fl_str_mv 2015-02-06T16:16:35Z
dc.date.available.fl_str_mv 2015-02-06T16:16:35Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
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dc.identifier.citation.fl_str_mv ZOLINI, Guilherme Pimenta et al. Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia. Zolini et al. Journal of Neuroinflammation, v.11, p. 20, 2014.
dc.identifier.uri.fl_str_mv https://www.arca.fiocruz.br/handle/icict/9450
dc.identifier.issn.none.fl_str_mv 1742-2094
dc.identifier.doi.none.fl_str_mv 10.1186/1742-2094-11-20
identifier_str_mv ZOLINI, Guilherme Pimenta et al. Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia. Zolini et al. Journal of Neuroinflammation, v.11, p. 20, 2014.
1742-2094
10.1186/1742-2094-11-20
url https://www.arca.fiocruz.br/handle/icict/9450
dc.language.iso.fl_str_mv eng
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dc.publisher.none.fl_str_mv Biomed Central
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