Effects of Anti-IL-17 on Inflammation, Remodeling, and Oxidative Stress in an Experimental Model of Asthma Exacerbated by LPS

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorCAMARGO, Leandro do Nascimento
dc.contributor.authorRIGHETTI, Renato Fraga
dc.contributor.authorARISTOTELES, Luciana Ritha de Cassia Rolim Barbosa
dc.contributor.authorSANTOS, Tabata Maruyama dos
dc.contributor.authorSOUZA, Flavia Castro Ribas de
dc.contributor.authorFUKUZAKI, Silvia
dc.contributor.authorCRUZ, Maysa Mariana
dc.contributor.authorALONSO-VALE, Maria Isabel Cardoso
dc.contributor.authorSARAIVA-ROMANHOLO, Beatriz Mangueira
dc.contributor.authorPRADO, Carla Maximo
dc.contributor.authorMARTINS, Milton de Arruda
dc.contributor.authorLEICK, Aparecida
dc.contributor.authorTIBERIO, Iolanda de Fatima Lopes Calvo
dc.date.accessioned2018-02-02T16:53:24Z
dc.date.available2018-02-02T16:53:24Z
dc.date.issued2018
dc.description.abstractInflammation plays a central role in the development of asthma, which is considered an allergic disease with a classic Th2 inflammatory profile. However, cytokine IL-17 has been examined to better understand the pathophysiology of this disease. Severe asthmatic patients experience frequent exacerbations, leading to infection, and subsequently show altered levels of inflammation that are unlikely to be due to the Th2 immune response alone. This study estimates the effects of anti-IL-17 therapy in the pulmonary parenchyma in a murine asthma model exacerbated by LPS. BALB/c mice were sensitized with intraperitoneal ovalbumin and repeatedly exposed to inhalation with ovalbumin, followed by treatment with or without anti-IL-17. Twenty-four hours prior to the end of the 29-day experimental protocol, the two groups received LPS (0.1 mg/ml intratracheal OVA-LPS and OVA-LPS IL-17). We subsequently evaluated bronchoalveolar lavage fluid, performed a lung tissue morphometric analysis, and measured IL-6 gene expression. OVA-LPS-treated animals treated with anti-IL-17 showed decreased pulmonary inflammation, edema, oxidative stress, and extracellular matrix remodeling compared to the non-treated OVA and OVA-LPS groups (p < 0.05). The anti-IL-17 treatment also decreased the numbers of dendritic cells, FOXP3, NF-kappa B, and Rho kinase 1-and 2-positive cells compared to the non-treated OVA and OVA-LPS groups (p < 0.05). In conclusion, these data suggest that inhibition of IL-17 is a promising therapeutic avenue, even in exacerbated asthmatic patients, and significantly contributes to the control of Th1/Th2/Th17 inflammation, chemokine expression, extracellular matrix remodeling, and oxidative stress in a murine experimental asthma model exacerbated by LPS.
dc.description.indexPubMed
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2013/17944-1]
dc.description.sponsorshipNational Council of Scientific and the Technological Development (CNPq)
dc.description.sponsorshipLaboratory of Medical Investigations (LIM-20 FMUSP)
dc.identifier.citationFRONTIERS IN IMMUNOLOGY, v.8, article ID 1835, 14p, 2018
dc.identifier.doi10.3389/fimmu.2017.01835
dc.identifier.issn1664-3224
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/24894
dc.language.isoeng
dc.publisherFRONTIERS MEDIA SA
dc.relation.ispartofFrontiers in Immunology
dc.rightsopenAccess
dc.rights.holderCopyright FRONTIERS MEDIA SA
dc.subjectanti-IL-17
dc.subjectdistal lung
dc.subjectasthma
dc.subjectinflammation
dc.subjectLPS-exacerbated
dc.subject.otherallergic pulmonary inflammation
dc.subject.otherrho-kinase inhibition
dc.subject.otherlung-tissue mechanics
dc.subject.otherfactor-kappa-b
dc.subject.otherairway inflammation
dc.subject.othert-cells
dc.subject.otheroral tolerance
dc.subject.othersmooth-muscle
dc.subject.otherguinea-pigs
dc.subject.otherth17 cells
dc.subject.wosImmunology
dc.titleEffects of Anti-IL-17 on Inflammation, Remodeling, and Oxidative Stress in an Experimental Model of Asthma Exacerbated by LPS
dc.typearticle
dc.type.categoryoriginal article
dc.type.versionpublishedVersion
dspace.entity.typePublication
hcfmusp.author.externalCRUZ, Maysa Mariana:Univ Fed Sao Paulo, Inst Biomed Sci, Dept Biol Sci, Sao Paulo, Brazil
hcfmusp.author.externalALONSO-VALE, Maria Isabel Cardoso:Univ Fed Sao Paulo, Inst Biomed Sci, Dept Biol Sci, Sao Paulo, Brazil
hcfmusp.author.externalPRADO, Carla Maximo:Univ Fed Sao Paulo, Dept Biol Sci, Sao Paulo, Brazil
hcfmusp.contributor.author-fmusphcLEANDRO DO NASCIMENTO CAMARGO
hcfmusp.contributor.author-fmusphcRENATO FRAGA RIGHETTI
hcfmusp.contributor.author-fmusphcLUCIANA RITHA DE CASSIA ROLIM BARBOSA ARISTOTELES
hcfmusp.contributor.author-fmusphcTABATA MARUYAMA DOS SANTOS
hcfmusp.contributor.author-fmusphcFLAVIA CASTRO RIBAS DE SOUZA
hcfmusp.contributor.author-fmusphcSILVIA FUKUZAKI
hcfmusp.contributor.author-fmusphcBEATRIZ MANGUEIRA SARAIVA RAMANHOLO
hcfmusp.contributor.author-fmusphcMILTON DE ARRUDA MARTINS
hcfmusp.contributor.author-fmusphcEDNA APARECIDA LEICK
hcfmusp.contributor.author-fmusphcIOLANDA DE FATIMA LOPES CALVO TIBERIO
hcfmusp.description.articlenumber1835
hcfmusp.description.volume8
hcfmusp.origemWOS
hcfmusp.origem.pubmed29379497
hcfmusp.origem.wosWOS:000419371800001
hcfmusp.publisher.cityLAUSANNE
hcfmusp.publisher.countrySWITZERLAND
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