Reactive oxygen species are involved in eosinophil extracellular traps release and in airway inflammation in asthma |
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Authors: | Josiane Silva Silveira Géssica Luana Antunes Daniela Benvenutti Kaiber Mariana Severo da Costa Eduardo Peil Marques Fernanda Silva Ferreira Rodrigo Benedetti Gassen Ricardo Vaz Breda Angela T S Wyse Paulo Pitrez Aline Andrea da Cunha |
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Institution: | 1. Department of Biochemistry, Laboratory of Neuroprotection and Neurometabolic Disease, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil;2. Laboratory of Pediatric Respirology, Infant Center, Medicine School, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil;3. Laboratory of Cellular and Molecular Immunology, Science School, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, Brazil;4. Institute of the Brain (INSCER), Medicine School, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Porto Alegre, RS, Brazil |
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Abstract: | In asthma, there are high levels of inflammatory mediators, reactive oxygen species (ROS), and eosinophil extracellular traps (EETs) formation in airway. Here, we attempted to investigate the ROS involvement in EETs release and airway inflammation in OVA-challenged mice. Before the intranasal challenge with ovalbumin (OVA), animals were treated with two ROS inhibitors, N-acetylcysteine (NAC) or diphenyleneiodonium (DPI). We showed that NAC treatment reduced inflammatory cells in lung. DPI and NAC treatments reduced eosinophil peroxidase (EPO), goblet cells hyperplasia, proinflammatory cytokines, NFκB p65 immunocontent, and oxidative stress in lung. However, only the NAC treatment improved mitochondrial energy metabolism. Moreover, the treatments with DPI and NAC reduced EETs release in airway. This is the first study to show that ROS are needed for EETs formation in asthma. Based on our results, NAC and DPI treatments can be an interesting alternative for reducing airway inflammation, mitochondrial damage, and EETs release in asthma. |
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Keywords: | diphenyleneiodonium DNA extracellular traps experimental asthma N-acetylcysteine oxidative stress |
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