Impacto da galectina-3 no curso da infecção experimental por Trypanosoma cruzi
Autor(a) principal: | |
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Data de Publicação: | 2015 |
Tipo de documento: | Dissertação |
Idioma: | por |
Título da fonte: | Repositório Institucional da UFU |
Texto Completo: | https://repositorio.ufu.br/handle/123456789/12404 https://doi.org/10.14393/ufu.di.2015.13 |
Resumo: | Galectin-3 (Gal-3) is a protein of the lectin-family, has affinity for β-galactose-containing carbohydrates, and can be localized in nucleus, cytoplasm, membrane associated or secreted. This protein is involved in many immunoregulatory processes, such as DC/T lymphocyte adhesion, inflammatory responses and cell migration toward inflammatory foci and cell proliferation. It was also seen that the T. cruzi infection, that is the etiological agent of Chagas disease, increases the expression of Gal-3. Thus, in this paper we aim to explore the biological activities of galectin-3 in acute and chronic T. cruzi experimental infection. Mice C57/BL6 Wild-Type (WT) and galectin-3 knockout (Gal-3KO) were infected intraperitoneally and was evaluate parasitaemia, recruitment of inflammatory cells in the peritoneal cavity, production of cytokines in spleen and heart and cardiac fibrosis. The data presented here demonstrate that the lack of Galectin-3 enhanced the parasitaemia and reduced the recruitment of leukocytes. In heart samples, we observed an increased secretion of TNF-α and IFN-γ in WT while in galectin-3 knockout mice we detected increased production of IL-1β and IL-4 during the acute phase. This scenario may have accounted to the higher infection rate during acute infection observed in knockout mice. We observed that in the chronic phase of infection the heart tissue of WT mice showed an immune response to Th2 profile, important to control tissue damage, with basal levels of IFN-γ and TNF-α, decrease in the concentration of IL-1β and increased IL-4. The increase in IL-4 is important for reducing heart damage and was not observed in animals Gal-3 KO. In chronic phase we observed an increased recruitment of mastocyte in Gal-3 KO animals and larger fibrosis of the heart. Therefore, the Gal-3 showed chemotactic and immunoregulatory functions that are needed to control the acute phase of infection and decreased chronic heart damage. |
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Impacto da galectina-3 no curso da infecção experimental por Trypanosoma cruziGalectina-3T. cruziResposta imuneLectinasTrypanosoma CruziImmune responseCNPQ::CIENCIAS BIOLOGICAS::MORFOLOGIA::CITOLOGIA E BIOLOGIA CELULARGalectin-3 (Gal-3) is a protein of the lectin-family, has affinity for β-galactose-containing carbohydrates, and can be localized in nucleus, cytoplasm, membrane associated or secreted. This protein is involved in many immunoregulatory processes, such as DC/T lymphocyte adhesion, inflammatory responses and cell migration toward inflammatory foci and cell proliferation. It was also seen that the T. cruzi infection, that is the etiological agent of Chagas disease, increases the expression of Gal-3. Thus, in this paper we aim to explore the biological activities of galectin-3 in acute and chronic T. cruzi experimental infection. Mice C57/BL6 Wild-Type (WT) and galectin-3 knockout (Gal-3KO) were infected intraperitoneally and was evaluate parasitaemia, recruitment of inflammatory cells in the peritoneal cavity, production of cytokines in spleen and heart and cardiac fibrosis. The data presented here demonstrate that the lack of Galectin-3 enhanced the parasitaemia and reduced the recruitment of leukocytes. In heart samples, we observed an increased secretion of TNF-α and IFN-γ in WT while in galectin-3 knockout mice we detected increased production of IL-1β and IL-4 during the acute phase. This scenario may have accounted to the higher infection rate during acute infection observed in knockout mice. We observed that in the chronic phase of infection the heart tissue of WT mice showed an immune response to Th2 profile, important to control tissue damage, with basal levels of IFN-γ and TNF-α, decrease in the concentration of IL-1β and increased IL-4. The increase in IL-4 is important for reducing heart damage and was not observed in animals Gal-3 KO. In chronic phase we observed an increased recruitment of mastocyte in Gal-3 KO animals and larger fibrosis of the heart. Therefore, the Gal-3 showed chemotactic and immunoregulatory functions that are needed to control the acute phase of infection and decreased chronic heart damage.Mestre em Biologia Celular e Estrutural AplicadasA galectina-3 (Gal-3) é uma proteína que pertence à família lectina, apresenta afinidade a carboidratos contendo β-galactosídeos, e pode estar localizada no núcleo, citoplasma, associada à membrana ou secretada. Esta proteína está envolvida em muitos processos imunoregulatórios, tais como adesão de linfócitos T/CD, respostas inflamatórias, migração de células para focos inflamatórios e proliferação celular. Foi visto que a infecção por Trypanosoma cruzi, agente etiológico da doença de Chagas, aumenta a expressão de Gal-3. Assim, o objetivo do trabalho foi explorar as atividades biológicas da Gal-3 nas fases aguda e crônica da infecção experimental por T. cruzi. . Camundongos C57 / BL6 Wild-Type (WT) e galectina-3 knockout (Gal-3 KO) foram infectados por via intraperitoneal e foram avaliados quanto a parasitemia, recrutamento de células inflamatórias na cavidade peritoneal, produção de citocinas do baço e coração e fibrose cardíaca. Os dados aqui apresentados demonstraram que a falta de Gal-3 aumentou a parasitemia e reduziu o recrutamento de leucócitos. Em amostras de coração, verificamos um aumento da secreção de TNF-α e IFN-γ em animais WT, enquanto que em animais Gal-3 KO foi detectado o aumento da produção de IL-1β e IL-4 durante a fase aguda. Este cenário pode ter sido responsável pela maior taxa de infecção durante a infecção aguda observada em camundongos deficientes em Gal-3. Observamos que na fase crônica da infecção o tecido cardíaco de camundongos WT apresentou uma resposta imune com perfil Th2, importante para o controle do dano tecidual, com níveis basais de TNF-α e IFN-γ, diminuição na concentração de IL-1β e aumento de IL-4. O aumento de IL-4 é importante para diminuir danos cardíacos e não foi observado em animais Gal-3 KO. Na fase crônica, observou-se um aumento de recrutamento de mastócitos em animais Gal-3 KO e maior fibrose do órgão. Portanto, a Gal-3 apresentou funções quimiotáticas e imunorreguladoras que são necessários para controlar a fase aguda da infecção e diminuir o comprometimento cardíaco na fase crônica.Universidade Federal de UberlândiaBRPrograma de Pós-graduação em Biologia Celular e Estrutural AplicadasCiências BiomédicasUFUTomiosso, Tatiana Carlahttp://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4777986P3Silva, Claudio Vieira dahttp://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4704340J2Gomes, Angelica de Oliveirahttp://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4736460H6Pereira, Fernando Lourençohttp://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4777988Z2Silva, Aline Alves da2016-06-22T18:31:53Z2015-03-102016-06-22T18:31:53Z2015-01-30info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/masterThesisapplication/pdfapplication/pdfSILVA, Aline Alves da. Impacto da galectina-3 no curso da infecção experimental por Trypanosoma cruzi. 2015. 104 f. Dissertação (Mestrado em Ciências Biomédicas) - Universidade Federal de Uberlândia, Uberlândia, 2015. DOI https://doi.org/10.14393/ufu.di.2015.13https://repositorio.ufu.br/handle/123456789/12404https://doi.org/10.14393/ufu.di.2015.13porinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFUinstname:Universidade Federal de Uberlândia (UFU)instacron:UFU2021-10-18T17:53:23Zoai:repositorio.ufu.br:123456789/12404Repositório InstitucionalONGhttp://repositorio.ufu.br/oai/requestdiinf@dirbi.ufu.bropendoar:2021-10-18T17:53:23Repositório Institucional da UFU - Universidade Federal de Uberlândia (UFU)false |
dc.title.none.fl_str_mv |
Impacto da galectina-3 no curso da infecção experimental por Trypanosoma cruzi |
title |
Impacto da galectina-3 no curso da infecção experimental por Trypanosoma cruzi |
spellingShingle |
Impacto da galectina-3 no curso da infecção experimental por Trypanosoma cruzi Silva, Aline Alves da Galectina-3 T. cruzi Resposta imune Lectinas Trypanosoma Cruzi Immune response CNPQ::CIENCIAS BIOLOGICAS::MORFOLOGIA::CITOLOGIA E BIOLOGIA CELULAR |
title_short |
Impacto da galectina-3 no curso da infecção experimental por Trypanosoma cruzi |
title_full |
Impacto da galectina-3 no curso da infecção experimental por Trypanosoma cruzi |
title_fullStr |
Impacto da galectina-3 no curso da infecção experimental por Trypanosoma cruzi |
title_full_unstemmed |
Impacto da galectina-3 no curso da infecção experimental por Trypanosoma cruzi |
title_sort |
Impacto da galectina-3 no curso da infecção experimental por Trypanosoma cruzi |
author |
Silva, Aline Alves da |
author_facet |
Silva, Aline Alves da |
author_role |
author |
dc.contributor.none.fl_str_mv |
Tomiosso, Tatiana Carla http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4777986P3 Silva, Claudio Vieira da http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4704340J2 Gomes, Angelica de Oliveira http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4736460H6 Pereira, Fernando Lourenço http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4777988Z2 |
dc.contributor.author.fl_str_mv |
Silva, Aline Alves da |
dc.subject.por.fl_str_mv |
Galectina-3 T. cruzi Resposta imune Lectinas Trypanosoma Cruzi Immune response CNPQ::CIENCIAS BIOLOGICAS::MORFOLOGIA::CITOLOGIA E BIOLOGIA CELULAR |
topic |
Galectina-3 T. cruzi Resposta imune Lectinas Trypanosoma Cruzi Immune response CNPQ::CIENCIAS BIOLOGICAS::MORFOLOGIA::CITOLOGIA E BIOLOGIA CELULAR |
description |
Galectin-3 (Gal-3) is a protein of the lectin-family, has affinity for β-galactose-containing carbohydrates, and can be localized in nucleus, cytoplasm, membrane associated or secreted. This protein is involved in many immunoregulatory processes, such as DC/T lymphocyte adhesion, inflammatory responses and cell migration toward inflammatory foci and cell proliferation. It was also seen that the T. cruzi infection, that is the etiological agent of Chagas disease, increases the expression of Gal-3. Thus, in this paper we aim to explore the biological activities of galectin-3 in acute and chronic T. cruzi experimental infection. Mice C57/BL6 Wild-Type (WT) and galectin-3 knockout (Gal-3KO) were infected intraperitoneally and was evaluate parasitaemia, recruitment of inflammatory cells in the peritoneal cavity, production of cytokines in spleen and heart and cardiac fibrosis. The data presented here demonstrate that the lack of Galectin-3 enhanced the parasitaemia and reduced the recruitment of leukocytes. In heart samples, we observed an increased secretion of TNF-α and IFN-γ in WT while in galectin-3 knockout mice we detected increased production of IL-1β and IL-4 during the acute phase. This scenario may have accounted to the higher infection rate during acute infection observed in knockout mice. We observed that in the chronic phase of infection the heart tissue of WT mice showed an immune response to Th2 profile, important to control tissue damage, with basal levels of IFN-γ and TNF-α, decrease in the concentration of IL-1β and increased IL-4. The increase in IL-4 is important for reducing heart damage and was not observed in animals Gal-3 KO. In chronic phase we observed an increased recruitment of mastocyte in Gal-3 KO animals and larger fibrosis of the heart. Therefore, the Gal-3 showed chemotactic and immunoregulatory functions that are needed to control the acute phase of infection and decreased chronic heart damage. |
publishDate |
2015 |
dc.date.none.fl_str_mv |
2015-03-10 2015-01-30 2016-06-22T18:31:53Z 2016-06-22T18:31:53Z |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/masterThesis |
format |
masterThesis |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
SILVA, Aline Alves da. Impacto da galectina-3 no curso da infecção experimental por Trypanosoma cruzi. 2015. 104 f. Dissertação (Mestrado em Ciências Biomédicas) - Universidade Federal de Uberlândia, Uberlândia, 2015. DOI https://doi.org/10.14393/ufu.di.2015.13 https://repositorio.ufu.br/handle/123456789/12404 https://doi.org/10.14393/ufu.di.2015.13 |
identifier_str_mv |
SILVA, Aline Alves da. Impacto da galectina-3 no curso da infecção experimental por Trypanosoma cruzi. 2015. 104 f. Dissertação (Mestrado em Ciências Biomédicas) - Universidade Federal de Uberlândia, Uberlândia, 2015. DOI https://doi.org/10.14393/ufu.di.2015.13 |
url |
https://repositorio.ufu.br/handle/123456789/12404 https://doi.org/10.14393/ufu.di.2015.13 |
dc.language.iso.fl_str_mv |
por |
language |
por |
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info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Universidade Federal de Uberlândia BR Programa de Pós-graduação em Biologia Celular e Estrutural Aplicadas Ciências Biomédicas UFU |
publisher.none.fl_str_mv |
Universidade Federal de Uberlândia BR Programa de Pós-graduação em Biologia Celular e Estrutural Aplicadas Ciências Biomédicas UFU |
dc.source.none.fl_str_mv |
reponame:Repositório Institucional da UFU instname:Universidade Federal de Uberlândia (UFU) instacron:UFU |
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Universidade Federal de Uberlândia (UFU) |
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UFU |
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UFU |
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Repositório Institucional da UFU |
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Repositório Institucional da UFU |
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Repositório Institucional da UFU - Universidade Federal de Uberlândia (UFU) |
repository.mail.fl_str_mv |
diinf@dirbi.ufu.br |
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