Reactive oxygen species are involved in eosinophil extracellular traps release and in airway inflammation in asthma.
Josiane Silva SilveiraGéssica Luana AntunesDaniela Benvenutti KaiberMariana Severo da CostaEduardo Peil MarquesFernanda Silva FerreiraRodrigo Benedetti GassenRicardo Vaz BredaAngela T S WysePaulo PitrezAline Andrea da CunhaPublished in: Journal of cellular physiology (2019)
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.
Keyphrases
- reactive oxygen species
- oxidative stress
- transcription factor
- induced apoptosis
- dna damage
- chronic obstructive pulmonary disease
- lung function
- cell death
- allergic rhinitis
- genome wide analysis
- cell cycle arrest
- signaling pathway
- diabetic rats
- ischemia reperfusion injury
- type diabetes
- cystic fibrosis
- skeletal muscle
- combination therapy
- metabolic syndrome
- lps induced
- nitric oxide
- inflammatory response
- cell proliferation
- nuclear factor
- newly diagnosed
- heat shock protein