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Autophagy induces eosinophil extracellular traps formation and allergic airway inflammation in a murine asthma model
Author(s) -
Silveira Josiane Silva,
Antunes Géssica Luana,
Kaiber Daniela Benvenutti,
da Costa Mariana Severo,
Ferreira Fernanda Silva,
Marques Eduardo Peil,
Schmitz Felipe,
Gassen Rodrigo Benedetti,
Breda Ricardo Vaz,
Wyse Angela T. S.,
Stein Renato Tetelbom,
Pitrez Paulo Márcio,
da Cunha Aline Andrea
Publication year - 2020
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.28966
Subject(s) - eosinophil , autophagy , asthma , inflammation , neutrophil extracellular traps , allergic inflammation , allergic asthma , immunology , extracellular , medicine , microbiology and biotechnology , biology , apoptosis , biochemistry
Studies have shown autophagy participation in the immunopathology of inflammatory diseases. However, autophagy role in asthma and in eosinophil extracellular traps (EETs) release is poorly understood. Here, we attempted to investigate the autophagy involvement in EETs release and in lung inflammation in an experimental asthma model. Mice were sensitized with ovalbumin (OVA), followed by OVA challenge. Before the challenge with OVA, mice were treated with an autophagy inhibitor, 3‐methyladenine (3‐MA). We showed that 3‐MA treatment decreases the number of eosinophils, eosinophil peroxidase (EPO) activity, goblet cells hyperplasia, proinflammatory cytokines, and nuclear factor kappa B (NFκB) p65 immunocontent in the lung. Moreover, 3‐MA was able to improve oxidative stress, mitochondrial energy metabolism, and Na + , K + ‐ATPase activity. We demonstrated that treatment with autophagy inhibitor 3‐MA reduced EETs formation in the airway. On the basis of our results, 3‐MA treatment can be an interesting alternative for reducing lung inflammation, oxidative stress, mitochondrial damage, and EETs formation in asthma.