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Please use this identifier to cite or link to this item: http://hdl.handle.net/1843/56335
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dc.creatorNathália Luísa Sousa de Oliveira Malaccopt_BR
dc.creatorFrederico Marianetti Sorianipt_BR
dc.creatorMilene Alvarenga Rachidpt_BR
dc.creatorIsabella Luisa da Silva Gurgelpt_BR
dc.creatorTauany Rodrigues Mourapt_BR
dc.creatorPedro Henrique Ferreira Sucupirapt_BR
dc.creatorLirlândia Pires de Sousapt_BR
dc.creatorDaniele da Glória de Souzapt_BR
dc.creatorRemo de Castro Russopt_BR
dc.creatorMauro Martins Teixeirapt_BR
dc.date.accessioned2023-07-14T22:48:55Z-
dc.date.available2023-07-14T22:48:55Z-
dc.date.issued2019-
dc.citation.volume8pt_BR
dc.citation.spage1pt_BR
dc.citation.epage13pt_BR
dc.identifier.doihttps://doi.org/10.3389/fcimb.2018.00453pt_BR
dc.identifier.issn2235-2988pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/56335-
dc.description.resumoAspergillus 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.pt_BR
dc.languageporpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentFAR - DEPARTAMENTO DE ANÁLISES CLÍNICAS E TOXICOLÓGICASpt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE BIOQUÍMICA E IMUNOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE FARMACOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE FISIOLOGIA E BIOFÍSICApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE PATOLOGIApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofFrontiers in Cellular and Infection Microbiologypt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectEosinophils role in inflammationpt_BR
dc.subjectFungal infectionpt_BR
dc.subjectInnate immunitypt_BR
dc.subjectIL-17 innate responsept_BR
dc.subjectEosinophil lung damagept_BR
dc.subject.otherEosinofilospt_BR
dc.subject.otherInfecçãopt_BR
dc.subject.otherImunidadept_BR
dc.titleEosinophil-Associated Innate IL-17 response promotes Aspergillus fumigatus Lung Pathologypt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.frontiersin.org/articles/10.3389/fcimb.2018.00453/fullpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-5823-2184pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-4720-6746pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-3142-6552pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-1797-6080pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-2778-7221pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-1997-1590pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-1042-9762pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-1715-3834pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6944-3008pt_BR
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