Eosinophil-Associated Innate IL-17 response promotes Aspergillus fumigatus Lung Pathology
Autor(a) principal: | |
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Data de Publicação: | 2019 |
Outros Autores: | , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | por |
Título da fonte: | Repositório Institucional da UFMG |
Texto Completo: | https://doi.org/10.3389/fcimb.2018.00453 http://hdl.handle.net/1843/56335 https://orcid.org/0000-0002-5823-2184 https://orcid.org/0000-0003-4720-6746 https://orcid.org/0000-0002-3142-6552 https://orcid.org/0000-0002-1797-6080 https://orcid.org/0000-0003-2778-7221 https://orcid.org/0000-0002-1997-1590 https://orcid.org/0000-0002-1042-9762 https://orcid.org/0000-0002-1715-3834 https://orcid.org/0000-0002-6944-3008 |
Resumo: | Aspergillus fumigatus is a common widespread microorganism with environmental, biological and clinical relevance. After inhalation, swollen conidia can germinate, colonize and invade pulmonary tissues. Eosinophils have been described as key cells in A. fumigatus lung infection. However, their specific role in protecting or damaging lung tissue as well as their relatioship among different A. fumigatus strains is poorly understood. Previously, it has been reported that eosinophils are able to produce IL17 and mediate an innate response that protected mice from infection using Af293 and CEA10 strains. Here, we have developed a set of new experiments with the CEA17-derived A1163 strain of A. fumigatus. Using 1dblGATA1 mice, we demonstrate that eosinophils produce IL-17 and are involved in control of neutrophil, macrophage and lymphocyte recruitment. We found that eosinophils also induce high levels of cytokines and chemokines, generating an intense inflammatory process. Eosinophils are responsible for increased pulmonary dysfunction and elevated lethality rates in mice. Curiously, fungal burden was not affected. To address the role of IL-17 signaling, pharmacological inhibition of this mediator in the airways with anti-IL-17 antibody was able to reduce inflammation in the airways and protect infected mice. In conclusion, our results demonstrate that eosinophils control IL-17-mediated response and contribute to lung pathology after A. fumigatus infection. Therefore, eosinophils may represent a potential target for controlling exacerbated inflammation and prevent tissue damage during this fungal infection. |
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Eosinophil-Associated Innate IL-17 response promotes Aspergillus fumigatus Lung PathologyEosinophils role in inflammationFungal infectionInnate immunityIL-17 innate responseEosinophil lung damageEosinofilosInfecçãoImunidadeAspergillus fumigatus is a common widespread microorganism with environmental, biological and clinical relevance. After inhalation, swollen conidia can germinate, colonize and invade pulmonary tissues. Eosinophils have been described as key cells in A. fumigatus lung infection. However, their specific role in protecting or damaging lung tissue as well as their relatioship among different A. fumigatus strains is poorly understood. Previously, it has been reported that eosinophils are able to produce IL17 and mediate an innate response that protected mice from infection using Af293 and CEA10 strains. Here, we have developed a set of new experiments with the CEA17-derived A1163 strain of A. fumigatus. Using 1dblGATA1 mice, we demonstrate that eosinophils produce IL-17 and are involved in control of neutrophil, macrophage and lymphocyte recruitment. We found that eosinophils also induce high levels of cytokines and chemokines, generating an intense inflammatory process. Eosinophils are responsible for increased pulmonary dysfunction and elevated lethality rates in mice. Curiously, fungal burden was not affected. To address the role of IL-17 signaling, pharmacological inhibition of this mediator in the airways with anti-IL-17 antibody was able to reduce inflammation in the airways and protect infected mice. In conclusion, our results demonstrate that eosinophils control IL-17-mediated response and contribute to lung pathology after A. fumigatus infection. Therefore, eosinophils may represent a potential target for controlling exacerbated inflammation and prevent tissue damage during this fungal infection.Universidade Federal de Minas GeraisBrasilFAR - DEPARTAMENTO DE ANÁLISES CLÍNICAS E TOXICOLÓGICASICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIAICB - DEPARTAMENTO DE FARMACOLOGIAICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICAICB - DEPARTAMENTO DE PATOLOGIAUFMG2023-07-14T22:48:55Z2023-07-14T22:48:55Z2019info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleapplication/pdfhttps://doi.org/10.3389/fcimb.2018.004532235-2988http://hdl.handle.net/1843/56335https://orcid.org/0000-0002-5823-2184https://orcid.org/0000-0003-4720-6746https://orcid.org/0000-0002-3142-6552https://orcid.org/0000-0002-1797-6080https://orcid.org/0000-0003-2778-7221https://orcid.org/0000-0002-1997-1590https://orcid.org/0000-0002-1042-9762https://orcid.org/0000-0002-1715-3834https://orcid.org/0000-0002-6944-3008porFrontiers in Cellular and Infection MicrobiologyNathália Luísa Sousa de Oliveira MalaccoFrederico Marianetti SorianiMilene Alvarenga RachidIsabella Luisa da Silva GurgelTauany Rodrigues MouraPedro Henrique Ferreira SucupiraLirlândia Pires de SousaDaniele da Glória de SouzaRemo de Castro RussoMauro Martins Teixeirainfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UFMGinstname:Universidade Federal de Minas Gerais (UFMG)instacron:UFMG2023-07-14T22:48:55Zoai:repositorio.ufmg.br:1843/56335Repositório InstitucionalPUBhttps://repositorio.ufmg.br/oairepositorio@ufmg.bropendoar:2023-07-14T22:48:55Repositório Institucional da UFMG - Universidade Federal de Minas Gerais (UFMG)false |
dc.title.none.fl_str_mv |
Eosinophil-Associated Innate IL-17 response promotes Aspergillus fumigatus Lung Pathology |
title |
Eosinophil-Associated Innate IL-17 response promotes Aspergillus fumigatus Lung Pathology |
spellingShingle |
Eosinophil-Associated Innate IL-17 response promotes Aspergillus fumigatus Lung Pathology Nathália Luísa Sousa de Oliveira Malacco Eosinophils role in inflammation Fungal infection Innate immunity IL-17 innate response Eosinophil lung damage Eosinofilos Infecção Imunidade |
title_short |
Eosinophil-Associated Innate IL-17 response promotes Aspergillus fumigatus Lung Pathology |
title_full |
Eosinophil-Associated Innate IL-17 response promotes Aspergillus fumigatus Lung Pathology |
title_fullStr |
Eosinophil-Associated Innate IL-17 response promotes Aspergillus fumigatus Lung Pathology |
title_full_unstemmed |
Eosinophil-Associated Innate IL-17 response promotes Aspergillus fumigatus Lung Pathology |
title_sort |
Eosinophil-Associated Innate IL-17 response promotes Aspergillus fumigatus Lung Pathology |
author |
Nathália Luísa Sousa de Oliveira Malacco |
author_facet |
Nathália Luísa Sousa de Oliveira Malacco Frederico Marianetti Soriani Milene Alvarenga Rachid Isabella Luisa da Silva Gurgel Tauany Rodrigues Moura Pedro Henrique Ferreira Sucupira Lirlândia Pires de Sousa Daniele da Glória de Souza Remo de Castro Russo Mauro Martins Teixeira |
author_role |
author |
author2 |
Frederico Marianetti Soriani Milene Alvarenga Rachid Isabella Luisa da Silva Gurgel Tauany Rodrigues Moura Pedro Henrique Ferreira Sucupira Lirlândia Pires de Sousa Daniele da Glória de Souza Remo de Castro Russo Mauro Martins Teixeira |
author2_role |
author author author author author author author author author |
dc.contributor.author.fl_str_mv |
Nathália Luísa Sousa de Oliveira Malacco Frederico Marianetti Soriani Milene Alvarenga Rachid Isabella Luisa da Silva Gurgel Tauany Rodrigues Moura Pedro Henrique Ferreira Sucupira Lirlândia Pires de Sousa Daniele da Glória de Souza Remo de Castro Russo Mauro Martins Teixeira |
dc.subject.por.fl_str_mv |
Eosinophils role in inflammation Fungal infection Innate immunity IL-17 innate response Eosinophil lung damage Eosinofilos Infecção Imunidade |
topic |
Eosinophils role in inflammation Fungal infection Innate immunity IL-17 innate response Eosinophil lung damage Eosinofilos Infecção Imunidade |
description |
Aspergillus fumigatus is a common widespread microorganism with environmental, biological and clinical relevance. After inhalation, swollen conidia can germinate, colonize and invade pulmonary tissues. Eosinophils have been described as key cells in A. fumigatus lung infection. However, their specific role in protecting or damaging lung tissue as well as their relatioship among different A. fumigatus strains is poorly understood. Previously, it has been reported that eosinophils are able to produce IL17 and mediate an innate response that protected mice from infection using Af293 and CEA10 strains. Here, we have developed a set of new experiments with the CEA17-derived A1163 strain of A. fumigatus. Using 1dblGATA1 mice, we demonstrate that eosinophils produce IL-17 and are involved in control of neutrophil, macrophage and lymphocyte recruitment. We found that eosinophils also induce high levels of cytokines and chemokines, generating an intense inflammatory process. Eosinophils are responsible for increased pulmonary dysfunction and elevated lethality rates in mice. Curiously, fungal burden was not affected. To address the role of IL-17 signaling, pharmacological inhibition of this mediator in the airways with anti-IL-17 antibody was able to reduce inflammation in the airways and protect infected mice. In conclusion, our results demonstrate that eosinophils control IL-17-mediated response and contribute to lung pathology after A. fumigatus infection. Therefore, eosinophils may represent a potential target for controlling exacerbated inflammation and prevent tissue damage during this fungal infection. |
publishDate |
2019 |
dc.date.none.fl_str_mv |
2019 2023-07-14T22:48:55Z 2023-07-14T22:48:55Z |
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.uri.fl_str_mv |
https://doi.org/10.3389/fcimb.2018.00453 2235-2988 http://hdl.handle.net/1843/56335 https://orcid.org/0000-0002-5823-2184 https://orcid.org/0000-0003-4720-6746 https://orcid.org/0000-0002-3142-6552 https://orcid.org/0000-0002-1797-6080 https://orcid.org/0000-0003-2778-7221 https://orcid.org/0000-0002-1997-1590 https://orcid.org/0000-0002-1042-9762 https://orcid.org/0000-0002-1715-3834 https://orcid.org/0000-0002-6944-3008 |
url |
https://doi.org/10.3389/fcimb.2018.00453 http://hdl.handle.net/1843/56335 https://orcid.org/0000-0002-5823-2184 https://orcid.org/0000-0003-4720-6746 https://orcid.org/0000-0002-3142-6552 https://orcid.org/0000-0002-1797-6080 https://orcid.org/0000-0003-2778-7221 https://orcid.org/0000-0002-1997-1590 https://orcid.org/0000-0002-1042-9762 https://orcid.org/0000-0002-1715-3834 https://orcid.org/0000-0002-6944-3008 |
identifier_str_mv |
2235-2988 |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.relation.none.fl_str_mv |
Frontiers in Cellular and Infection Microbiology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Universidade Federal de Minas Gerais Brasil FAR - DEPARTAMENTO DE ANÁLISES CLÍNICAS E TOXICOLÓGICAS ICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIA ICB - DEPARTAMENTO DE FARMACOLOGIA ICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICA ICB - DEPARTAMENTO DE PATOLOGIA UFMG |
publisher.none.fl_str_mv |
Universidade Federal de Minas Gerais Brasil FAR - DEPARTAMENTO DE ANÁLISES CLÍNICAS E TOXICOLÓGICAS ICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIA ICB - DEPARTAMENTO DE FARMACOLOGIA ICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICA ICB - DEPARTAMENTO DE PATOLOGIA UFMG |
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reponame:Repositório Institucional da UFMG instname:Universidade Federal de Minas Gerais (UFMG) instacron:UFMG |
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Universidade Federal de Minas Gerais (UFMG) |
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UFMG |
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UFMG |
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Repositório Institucional da UFMG |
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Repositório Institucional da UFMG - Universidade Federal de Minas Gerais (UFMG) |
repository.mail.fl_str_mv |
repositorio@ufmg.br |
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1816829618683904000 |