Pharmacological modulation of reactive oxygen species (ROS) improves the airway hyperresponsiveness by shifting the Th1 response in allergic inflammation induced by ovalbumin

dc.creatorNesi, Renata Tiscoski
dc.creatorBarroso, Marina Valente
dc.creatorMuniz, Valdirene de Souza
dc.creatorArantes, Ana Carolina de
dc.creatorMartins, Marco Aurélio
dc.creatorGitirana, Lycia de Brito
dc.creatorNeves, Josiane Sabbadini
dc.creatorBenjamim, Cláudia Farias
dc.creatorLanzetti, Manuella
dc.creatorValenca, Samuel Santos
dc.date2017-12-11T10:28:17Z
dc.date2017-12-11T10:28:17Z
dc.date2017
dc.date.accessioned2023-09-26T20:38:22Z
dc.date.available2023-09-26T20:38:22Z
dc.identifierNESI, Renata Tiscoski; et al. Pharmacological modulation of reactive oxygen species (ROS) improves the airway hyperresponsiveness by shifting the Th1 response in allergic inflammation induced by ovalbumin. Free Radical Research, v.51, n.7-8, p.708-712, 2017.
dc.identifier1071-5762
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/23587
dc.identifier10.1080/10715762.2017.1364377
dc.identifier1029-2470
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8861109
dc.descriptionAsthma is an allergic inflammation driven by the Th2 immune response with release of cytokines such as IL-4 and IL-13, which contribute to the airflow limitations and airway hyperresponsiveness (AHR). The involvement of oxidative stress in this process is well-established, but the specific role of the superoxide anion and nitric oxide in asthma are poorly understood. Thus, the aim of this study was to investigate the mechanisms underlying the superoxide anion/nitric oxide production and detoxification in a murine asthma model. BALB/c male mice were sensitised and challenged with ovalbumin (OVA). Pretreatments with either apocynin (14 mg/kg) or allopurinol (25 mg/kg) (superoxide anion synthesis inhibitors), aminoguanidine (50 mg/kg) (nitric oxide synthesis inhibitor) or diethyldithiocarbamate (100 mg/kg) (superoxide dismutase inhibitor) were performed 1 h before the challenge. Our data showed that apocynin and allopurinol ameliorated AHR and reduced eosinophil peroxidase, as well as IL-4 and IL-13 levels. Apocynin also abrogated leukocyte peribronchiolar infiltrate and increased IL-1β secretion. Aminoguanidine preserved lung function and shifted the Th2 to the Th1 response with a reduction of IL-4 and IL-13 and increase in IL-1β production. Diethyldithiocarbamate prevented neither allergen-induced AHR nor eosinophil peroxidase (EPO) generation. All treatments protected against oxidative damage observed by a reduction in TBARS levels. Taken together, these results suggest that AHR in an asthma model can be avoided by the down-regulation of superoxide anion and nitric oxide synthesis in a mechanism that is independent of a redox response. This down-regulation is also associated with a transition in the typical immunological Th2 response toward the Th1 profile.
dc.description2030-01-01
dc.formatapplication/pdf
dc.languageeng
dc.publisherTaylor & Francis
dc.rightsrestricted access
dc.subjectAntioxidantes
dc.subjectRatos
dc.subjectÓxido nítrico
dc.subjectSuperóxidos
dc.subjectInflamação alérgica
dc.subjectAllergic inflammation
dc.subjectantioxidant
dc.subjectmice
dc.subjectnitric oxide
dc.subjectsuperoxide anion
dc.titlePharmacological modulation of reactive oxygen species (ROS) improves the airway hyperresponsiveness by shifting the Th1 response in allergic inflammation induced by ovalbumin
dc.typeArticle


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