Hydroquinone exposure worsens rheumatoid arthritis through the activation of the aryl hydrocarbon receptor and interleukin-17 pathways

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dc.creatorCintia Scucuglia Heluany
dc.creatorGiovanna Nalesso
dc.creatorEduardo Lani Volpe Silveira
dc.creatorFernando Queiroz Cunha
dc.creatorSandra Helena Poliselli Farsky
dc.creatorPaula Barbim Donate
dc.creatorAyda Henriques Schneider
dc.creatorAndré Luis Fabris
dc.creatorRenan Augusto Gomes
dc.creatorIsadora Maria Villas-boas
dc.creatorDenise Vilarinho Tambourgi
dc.creatorTarcília Aparecida da Silva
dc.creatorGustavo Henrique Goulart Trossini
dc.date.accessioned2025-04-29T20:50:45Z
dc.date.accessioned2025-09-09T00:22:30Z
dc.date.available2025-04-29T20:50:45Z
dc.date.issued2021
dc.description.sponsorshipFAPESP - Fundação de Amparo à Pesquisa do Estado de São Paulo
dc.format.mimetypepdf
dc.identifier.doihttps://doi.org/10.3390/antiox10060929
dc.identifier.issn2076-3921
dc.identifier.urihttps://hdl.handle.net/1843/81965
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofAntioxidants
dc.rightsAcesso Aberto
dc.subjectCigarette smoking
dc.subjectEnvironmental pollutants
dc.subjectArthritis, rheumatoid
dc.subjectReceptors, tumor necrosis factor, type I
dc.subjectReceptors, tumor necrosis factor, type II
dc.subjectReactive oxygen species
dc.subjectInterleukin-6
dc.subjectInterleukin-8
dc.subjectGene expression
dc.subjectSigns and symptoms
dc.subjectSynoviocytes
dc.subjectInterleukin-17
dc.subjectReceptors, aryl hydrocarbon
dc.subjectCell proliferation
dc.subject.otherEnvironmental pollutant
dc.subject.otherAntigen-induced arthritis
dc.subject.otherBenzene metabolite
dc.subject.otherCigarette smoking
dc.subject.otherFibroblast-like synoviocytes
dc.titleHydroquinone exposure worsens rheumatoid arthritis through the activation of the aryl hydrocarbon receptor and interleukin-17 pathways
dc.typeArtigo de periódico
local.citation.epage946
local.citation.issue6
local.citation.spage929
local.citation.volume10
local.description.resumoRheumatoid arthritis (RA) development is strongly associated with cigarette smoke exposure, which activates the aryl hydrocarbon receptor (AhR) as a trigger for Th17 inflammatory pathways. We previously demonstrated that the exposure to hydroquinone (HQ), one of the major compounds of cigarette tar, aggravates the arthritis symptomatology in rats. However, the mechanisms related to the HQ-related RA still remain elusive. Cell viability, cytokine secretion, and gene expression were measured in RA human fibroblast-like synoviocytes (RAHFLS) treated with HQ and stimulated or not with TNF-α. Antigen-induced arthritis (AIA) was also elicited in wild type (WT), AhR -/- or IL-17R -/- C57BL/6 mice upon daily exposure to nebulized HQ (25ppm) between days 15 to 21. At day 21, mice were challenged with mBSA and inflammatory parameters were assessed. The in vitro HQ treatment up-regulated TNFR1, TNFR2 expression, and increased ROS production. The co-treatment of HQ and TNF-α enhanced the IL-6 and IL-8 secretion. However, the pre-incubation of RAHFLS with an AhR antagonist inhibited the HQ-mediated cell proliferation and gene expression profile. About the in vivo approach, the HQ exposure worsened the AIA symptoms (edema, pain, cytokines secretion and NETs formation) in WT mice. These AIA effects were abolished in HQ-exposed AhR -/- and IL-17R -/- animals though. Our data demonstrated the harmful HQ influence over the onset of arthritis through the activation and proliferation of synoviocytes. The HQ-related RA severity was also associated with the activation of AhR and IL-17 pathways, highlighting how cigarette smoke compounds can contribute to the RA progression.
local.identifier.orcidhttps://orcid.org/0009-0006-0466-2724
local.identifier.orcidhttps://orcid.org/0000-0002-9424-3075
local.identifier.orcidhttps://orcid.org/0000-0001-8333-2884
local.identifier.orcidhttps://orcid.org/0000-0003-4755-1670
local.identifier.orcidhttps://orcid.org/0000-0002-3943-977X
local.identifier.orcidhttps://orcid.org/0000-0001-8422-8894
local.identifier.orcidhttps://orcid.org/0000-0003-2474-2773
local.identifier.orcidhttps://orcid.org/0000-0002-5173-4050
local.identifier.orcidhttps://orcid.org/0000-0002-4220-6838
local.identifier.orcidhttps://orcid.org/0000-0001-6034-9544
local.identifier.orcidhttps://orcid.org/0000-0003-1896-9074
local.identifier.orcidhttps://orcid.org/0000-0001-9623-7835
local.identifier.orcidhttps://orcid.org/0000-0003-3634-2531
local.publisher.countryBrasil
local.publisher.departmentFAO - DEPARTAMENTO DE CLÍNICA
local.publisher.initialsUFMG
local.url.externahttps://www.mdpi.com/2076-3921/10/6/929

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