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Cholinergic anti‐inflammatory pathway confers airway protection against oxidative damage and attenuates inflammation in an allergic asthma model
Author(s) -
Antunes Géssica Luana,
Silveira Josiane Silva,
Kaiber Daniela Benvenutti,
Luft Carolina,
da Costa Mariana Severo,
Marques Eduardo Peil,
Ferreira Fernanda Silva,
Breda Ricardo Vaz,
Wyse Angela T. S.,
Stein Renato Tetelbom,
Pitrez Paulo Márcio,
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.29101
Subject(s) - oxidative stress , reactive oxygen species , inflammation , neostigmine , immunology , asthma , cytokine , medicine , allergic inflammation , catalase , cholinergic , pharmacology , chemistry , endocrinology , biochemistry
Abstract Asthma is characterized by the influx of inflammatory cells, especially of eosinophils as well as reactive oxygen species (ROS) production, driven by the release of the T helper 2 (Th2)‐cell‐associated cytokines. The cholinergic anti‐inflammatory pathway (CAP) inhibit cytokines production and controls inflammation. Thus, we investigated the effects of pharmacological activation of CAP by neostigmine on oxidative stress and airway inflammation in an allergic asthma model. After the OVA challenge, mice were treated with neostigmine. We showed that CAP activation by neostigmine reduced the levels of pro‐inflammatory cytokines (IL‐4, IL‐5, IL‐13, IL‐1β, and TNF‐α), which resulted in a decrease of eosinophils influx. Furthermore, neostigmine also conferred airway protection against oxidative stress, attenuating ROS production through the increase of antioxidant defense, evidenced by the catalase (CAT) activity. We propose, for the first time, that pharmacological activation of the CAP can lead to new possibilities in the therapeutic management of allergic asthma.