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Reactive oxygen species are involved in eosinophil extracellular traps release and in airway inflammation in asthma
Author(s) -
Silveira Josiane Silva,
Antunes Géssica Luana,
Kaiber Daniela Benvenutti,
da Costa Mariana Severo,
Marques Eduardo Peil,
Ferreira Fernanda Silva,
Gassen Rodrigo Benedetti,
Breda Ricardo Vaz,
Wyse Angela T. S.,
Pitrez Paulo,
da Cunha Aline Andrea
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28931
Subject(s) - eosinophil , inflammation , asthma , reactive oxygen species , extracellular , immunology , airway , allergic inflammation , chemistry , medicine , biology , microbiology and biotechnology , anesthesia
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.