Montelukast reduces inhaled chlorine triggered airway hyperresponsiveness and airway inflammation in the mouse

What is it about?

Cysteinyl leukotrienes (cysLTs) are well known mediators involved in the pathogensis of allergic asthma. Less understood is the role of cysLTs in oxidative stress induced, non-allergic asthma. The goal of this study was to study the role of cysLTs following the inhalation of chlorine gas. Chlorine causes high levels of oxidative stress and induces airway inflammation and airway hyperresponsiveness (AHR). To assess the role of cysLTs during the response to chlorine ihalation, we used a cysLT1 receptor inhibitor, Montelukast (MK), and assessed airway inflammation, AHR, and the antioxidant response. We found that treatment with MK prevented airway inflammation and AHR as well as increases in pro-inflammatory cytokines, IL-6 and VEGF. We used antibodies against IL-6 and VEGF to determine the roles of these cytokines in the response to chlorine inhalation and found that IL-6, but not VEGF contributes to chlorine-induced AHR and inflammation.

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