Extracellular vesicles shed by Trypanosoma cruzi potentiate infection and elicit lipid body formation and PGE2 production in Murine Macrophages

Detalhes bibliográficos
Autor(a) principal: Lovo-Martins, Maria Isabel
Data de Publicação: 2018
Outros Autores: Malvezi, Aparecida Donizette, Zanluqui, Nágela Ghabdan, Lucchetti, Bruno Fernando Cruz, Tatakihara, Vera Lúcia Hideko, Morking, Patricia Alves, Oliveira, Admilton Gonçalves de, Goldenberg, Samuel, Wowk, Pryscilla Fanini, Pinge-Filho, Phileno
Tipo de documento: Artigo
Idioma: por
Título da fonte: Repositório Institucional da FIOCRUZ (ARCA)
Texto Completo: https://www.arca.fiocruz.br/handle/icict/28743
Resumo: Fundação Oswaldo Cruz. Instituto Carlos Chagas. Curitiba, PR, Brasil / Universidade Estadual de Londrina. Centro de Ciências Biológicas. Departamento de Ciências Patológicas. Laboratório de Imunopatologia Experimental. Londrina, PR, Brasil.
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spelling Lovo-Martins, Maria IsabelMalvezi, Aparecida DonizetteZanluqui, Nágela GhabdanLucchetti, Bruno Fernando CruzTatakihara, Vera Lúcia HidekoMorking, Patricia AlvesOliveira, Admilton Gonçalves deGoldenberg, SamuelWowk, Pryscilla FaniniPinge-Filho, Phileno2018-09-13T15:13:39Z2018-09-13T15:13:39Z2018LOVO-MARTINS, Maria Isabel et al. Extracellular vesicles shed by Trypanosoma cruzi potentiate infection and elicit lipid body formation and PGE2 production in Murine Macrophages. Frontiers in Immunology, v. 9, p. 1-16, 2018.1664-3224https://www.arca.fiocruz.br/handle/icict/2874310.3389/fimmu.2018.008961664-3224porFrontiers MediaVesículas ExtracelularesExtracellular VesiclesLipid DropletsMacrophagesProstaglandin E2Antigenic ModulationGotas LipídicasModulación AntigénicaGotículas LipídicasMacrófagosDinoprostonaModulação AntigênicaExtracellular vesicles shed by Trypanosoma cruzi potentiate infection and elicit lipid body formation and PGE2 production in Murine Macrophagesinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleFundação Oswaldo Cruz. Instituto Carlos Chagas. Curitiba, PR, Brasil / Universidade Estadual de Londrina. Centro de Ciências Biológicas. Departamento de Ciências Patológicas. Laboratório de Imunopatologia Experimental. Londrina, PR, Brasil.Universidade Estadual de Londrina. Centro de Ciências Biológicas. Departamento de Ciências Patológicas. Laboratório de Imunopatologia Experimental. Londrina, PR, Brasil.Fundação Oswaldo Cruz. Instituto Carlos Chagas. Curitiba, PR, Brasil.Universidade Estadual de Londrina. Centro de Ciências Biológicas. Departamento de Ciências Patológicas. Laboratório de Imunopatologia Experimental. Londrina, PR, Brasil.Universidade Estadual de Londrina. Centro de Ciências Biológicas. Departamento de Ciências Patológicas. Laboratório de Imunopatologia Experimental. Londrina, PR, Brasil.Fundação Oswaldo Cruz. Instituto Carlos Chagas. Curitiba, PR, Brasil.Universidade Estadual de Londrina. Central de Laboratórios de Pesquisa Multiusuários. Laboratório de Microscopia Eletrônica e Microanálises. Londrina, PR, Brasil.Fundação Oswaldo Cruz. Instituto Carlos Chagas. Curitiba, PR, Brasil.Fundação Oswaldo Cruz. Instituto Carlos Chagas. Laboratório de Virologia Molecular. Curitiba, PR, Brasil.Universidade Estadual de Londrina. Centro de Ciências Biológicas. Departamento de Ciências Patológicas. Laboratório de Imunopatologia Experimental. Londrina, PR, Brasil.During the onset of Trypanosoma cruzi infection, an effective immune response is necessary to control parasite replication and ensure host survival. Macrophages have a central role in innate immunity, acting as an important trypanocidal cell and triggering the adaptive immune response through antigen presentation and cytokine production. However, T. cruzi displays immune evasion mechanisms that allow infection and replication in macrophages, favoring its chronic persistence. One potential mechanism is the release of T. cruzi strain Y extracellular vesicle (EV Y), which participate in intracellular communication by carrying functional molecules that signal host cells and can modulate the immune response. The present work aimed to evaluate immune modulation by EV Y in C57BL/6 mice, a prototype resistant to infection by T. cruzi strain Y, and the effects of direct EV Y stimulation of macrophages in vitro. EV Y inoculation in mice prior to T. cruzi infection resulted in increased parasitemia, elevated cardiac parasitism, decreased plasma nitric oxide (NO), reduced NO production by spleen cells, and modulation of cytokine production, with a reduction in TNF-α in plasma and decreased production of TNF-α and IL-6 by spleen cells from infected animals. In vitro assays using bone marrow-derived macrophages showed that stimulation with EV Y prior to infection by T. cruzi increased the parasite internalization rate and release of infective trypomastigotes by these cells. In this same scenario, EV Y induced lipid body formation and prostaglandin E2 (PGE2) production by macrophages even in the absence of T. cruzi. In infected macrophages, EV Y decreased production of PGE2 and cytokines TNF-α and IL-6 24 h after infection. These results suggest that EV Y modulates the host response in favor of the parasite and indicates a role for lipid bodies and PGE2 in immune modulation exerted by EVs.info:eu-repo/semantics/openAccessreponame:Repositório Institucional da FIOCRUZ (ARCA)instname:Fundação Oswaldo Cruz (FIOCRUZ)instacron:FIOCRUZLICENSElicense.txtlicense.txttext/plain; charset=utf-83084https://www.arca.fiocruz.br/bitstream/icict/28743/1/license.txt783568c2893d2e25a99990b126be1772MD51ORIGINALFrontiersImmunol-09-896.pdfFrontiersImmunol-09-896.pdfapplication/pdf4388180https://www.arca.fiocruz.br/bitstream/icict/28743/2/FrontiersImmunol-09-896.pdf78f9ff8768a5eb707450f4233383949dMD52TEXTFrontiersImmunol-09-896.pdf.txtFrontiersImmunol-09-896.pdf.txtExtracted texttext/plain86458https://www.arca.fiocruz.br/bitstream/icict/28743/3/FrontiersImmunol-09-896.pdf.txtc32ea3030dcd1cdafc4b09edd5d06b8cMD53icict/287432019-11-23 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dc.title.pt_BR.fl_str_mv Extracellular vesicles shed by Trypanosoma cruzi potentiate infection and elicit lipid body formation and PGE2 production in Murine Macrophages
title Extracellular vesicles shed by Trypanosoma cruzi potentiate infection and elicit lipid body formation and PGE2 production in Murine Macrophages
spellingShingle Extracellular vesicles shed by Trypanosoma cruzi potentiate infection and elicit lipid body formation and PGE2 production in Murine Macrophages
Lovo-Martins, Maria Isabel
Vesículas Extracelulares
Extracellular Vesicles
Lipid Droplets
Macrophages
Prostaglandin E2
Antigenic Modulation
Gotas Lipídicas
Modulación Antigénica
Gotículas Lipídicas
Macrófagos
Dinoprostona
Modulação Antigênica
title_short Extracellular vesicles shed by Trypanosoma cruzi potentiate infection and elicit lipid body formation and PGE2 production in Murine Macrophages
title_full Extracellular vesicles shed by Trypanosoma cruzi potentiate infection and elicit lipid body formation and PGE2 production in Murine Macrophages
title_fullStr Extracellular vesicles shed by Trypanosoma cruzi potentiate infection and elicit lipid body formation and PGE2 production in Murine Macrophages
title_full_unstemmed Extracellular vesicles shed by Trypanosoma cruzi potentiate infection and elicit lipid body formation and PGE2 production in Murine Macrophages
title_sort Extracellular vesicles shed by Trypanosoma cruzi potentiate infection and elicit lipid body formation and PGE2 production in Murine Macrophages
author Lovo-Martins, Maria Isabel
author_facet Lovo-Martins, Maria Isabel
Malvezi, Aparecida Donizette
Zanluqui, Nágela Ghabdan
Lucchetti, Bruno Fernando Cruz
Tatakihara, Vera Lúcia Hideko
Morking, Patricia Alves
Oliveira, Admilton Gonçalves de
Goldenberg, Samuel
Wowk, Pryscilla Fanini
Pinge-Filho, Phileno
author_role author
author2 Malvezi, Aparecida Donizette
Zanluqui, Nágela Ghabdan
Lucchetti, Bruno Fernando Cruz
Tatakihara, Vera Lúcia Hideko
Morking, Patricia Alves
Oliveira, Admilton Gonçalves de
Goldenberg, Samuel
Wowk, Pryscilla Fanini
Pinge-Filho, Phileno
author2_role author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Lovo-Martins, Maria Isabel
Malvezi, Aparecida Donizette
Zanluqui, Nágela Ghabdan
Lucchetti, Bruno Fernando Cruz
Tatakihara, Vera Lúcia Hideko
Morking, Patricia Alves
Oliveira, Admilton Gonçalves de
Goldenberg, Samuel
Wowk, Pryscilla Fanini
Pinge-Filho, Phileno
dc.subject.other.pt_BR.fl_str_mv Vesículas Extracelulares
topic Vesículas Extracelulares
Extracellular Vesicles
Lipid Droplets
Macrophages
Prostaglandin E2
Antigenic Modulation
Gotas Lipídicas
Modulación Antigénica
Gotículas Lipídicas
Macrófagos
Dinoprostona
Modulação Antigênica
dc.subject.en.pt_BR.fl_str_mv Extracellular Vesicles
Lipid Droplets
Macrophages
Prostaglandin E2
Antigenic Modulation
dc.subject.es.pt_BR.fl_str_mv Gotas Lipídicas
Modulación Antigénica
dc.subject.decs.pt_BR.fl_str_mv Gotículas Lipídicas
Macrófagos
Dinoprostona
Modulação Antigênica
description Fundação Oswaldo Cruz. Instituto Carlos Chagas. Curitiba, PR, Brasil / Universidade Estadual de Londrina. Centro de Ciências Biológicas. Departamento de Ciências Patológicas. Laboratório de Imunopatologia Experimental. Londrina, PR, Brasil.
publishDate 2018
dc.date.accessioned.fl_str_mv 2018-09-13T15:13:39Z
dc.date.available.fl_str_mv 2018-09-13T15:13:39Z
dc.date.issued.fl_str_mv 2018
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.citation.fl_str_mv LOVO-MARTINS, Maria Isabel et al. Extracellular vesicles shed by Trypanosoma cruzi potentiate infection and elicit lipid body formation and PGE2 production in Murine Macrophages. Frontiers in Immunology, v. 9, p. 1-16, 2018.
dc.identifier.uri.fl_str_mv https://www.arca.fiocruz.br/handle/icict/28743
dc.identifier.issn.pt_BR.fl_str_mv 1664-3224
dc.identifier.doi.none.fl_str_mv 10.3389/fimmu.2018.00896
dc.identifier.eissn.none.fl_str_mv 1664-3224
identifier_str_mv LOVO-MARTINS, Maria Isabel et al. Extracellular vesicles shed by Trypanosoma cruzi potentiate infection and elicit lipid body formation and PGE2 production in Murine Macrophages. Frontiers in Immunology, v. 9, p. 1-16, 2018.
1664-3224
10.3389/fimmu.2018.00896
url https://www.arca.fiocruz.br/handle/icict/28743
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dc.publisher.none.fl_str_mv Frontiers Media
publisher.none.fl_str_mv Frontiers Media
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