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Pulmonary paracoccidioidomycosis in AhR deficient hosts is severe and associated with defective Treg and Th22 responses

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dc.contributor.authorde Araújo, Eliseu Frank
dc.contributor.authorPreite, Nycolas Willian
dc.contributor.authorVeldhoen, Marc
dc.contributor.authorLoures, Flávio Vieira
dc.contributor.authorCalich, Vera Lúcia Garcia
dc.date.accessioned2022-06-06T13:41:21Z
dc.date.available2022-06-06T13:41:21Z
dc.date.issued2020
dc.description© The Author(s) 2020. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.pt_PT
dc.description.abstractAhR is a ligand-activated transcription factor that plays an important role in the innate and adaptive immune responses. In infection models, it has been associated with host responses that promote or inhibit disease progression. In pulmonary paracoccidioidomycosis, a primary fungal infection endemic in Latin America, immune protection is mediated by Th1/Th17 cells and disease severity with predominant Th2/Th9/Treg responses. Because of its important role at epithelial barriers, we evaluate the role of AhR in the outcome of a pulmonary model of paracoccidioidomycosis. AhR-/- mice show increased fungal burdens, enhanced tissue pathology and mortality. During the infection, AhR-/- mice have more pulmonary myeloid cells with activated phenotype and reduced numbers expressing indoleamine 2,3 dioxygenase 1. AhR-deficient lungs have altered production of cytokines and reduced numbers of innate lymphoid cells (NK, ILC3 and NCR IL-22). The lungs of AhR-/- mice showed increased presence Th17 cells concomitant with reduced numbers of Th1, Th22 and Foxp3+ Treg cells. Furthermore, treatment of infected WT mice with an AhR-specific antagonist (CH223191) reproduced the main findings obtained in AhR-/- mice. Collectively our data demonstrate that in pulmonary paracoccidioidomycosis AhR controls fungal burden and excessive tissue inflammation and is a possible target for antifungal therapy.pt_PT
dc.description.sponsorshipThis work was supported by a grant from the Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP-grant to VLGC 2011/51258-2 and 2016/23189-0; fellowship to EFA 2014/18668-2; grant to FVL 2018/14762-3; fellowship to NWP 2019-09278-8), European Union H2020 ERA project (No 667824 – EXCELLtoINNOV) to MV and Conselho Nacional de Pesquisas (CNPq).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationSci Rep. 2020 Jul 9;10(1):11312pt_PT
dc.identifier.doi10.1038/s41598-020-68322-6pt_PT
dc.identifier.eissn2045-2322
dc.identifier.urihttp://hdl.handle.net/10451/53278
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherSpringer Naturept_PT
dc.relationLeverage research EXCELLence and INNOVation potential of Instituto de Medicina Molecular (IMM) through translational biomedical research in immunity and infection.
dc.relation.publisherversionhttps://www.nature.com/srep/pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.titlePulmonary paracoccidioidomycosis in AhR deficient hosts is severe and associated with defective Treg and Th22 responsespt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardNumber667824
oaire.awardTitleLeverage research EXCELLence and INNOVation potential of Instituto de Medicina Molecular (IMM) through translational biomedical research in immunity and infection.
oaire.awardURIinfo:eu-repo/grantAgreement/EC/H2020/667824/EU
oaire.citation.issue1pt_PT
oaire.citation.titleScientific Reportspt_PT
oaire.citation.volume10pt_PT
oaire.fundingStreamH2020
person.familyNameVeldhoen
person.givenNameMarc
person.identifierhttps://scholar.google.pt/citations?hl=en&user=7vG1jLIAAAAJ
person.identifier.ciencia-id6413-A3A0-C7AD
person.identifier.orcid0000-0002-1478-9562
person.identifier.scopus-author-id8323789000
project.funder.identifierhttp://doi.org/10.13039/501100008530
project.funder.nameEuropean Commission
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublicationb6ddef66-b6bb-4ce5-b68a-e4b211aa2411
relation.isAuthorOfPublication.latestForDiscoveryb6ddef66-b6bb-4ce5-b68a-e4b211aa2411
relation.isProjectOfPublication7a4a0b51-ecdc-4c02-9d2b-0ac079311b63
relation.isProjectOfPublication.latestForDiscovery7a4a0b51-ecdc-4c02-9d2b-0ac079311b63

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