Airway IL-33 levels are similar in current and former smokers with stable or exacerbating COPD

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Background: Anti-IL-33 monoclonal antibodies (mAb) have shown clinical efficacy in COPD patients; however, studies have shown contrasting results in current (CS) and former (FS) smokers. Although IL33 gene expression in the airways is suppressed in CS with COPD, expression of oxidized IL-33 (IL-33ox) signatures is increased. Objective: To assess the impact of smoking on IL-33 release in the airways of stable and exacerbating COPD patients. Methods: IL33 gene expression in bronchial brushings was measured using a gene array data.1 IL-33 protein was measured in sputum and nasal mucosal lining fluid (MLF) using immunoassays. Results: IL33 gene expression was lower in bronchial airway of COPD CS (n=38) than FS (n=56; 1.3-fold; p=0.005). In contrast, sputum levels of total free IL-33 were similar in CS and FS with stable COPD. Reduced IL-33 (IL-33red) and IL-33ox levels were similar in nasal MLF from CS and FS with COPD during viral exacerbations (Table). Conclusions: Comparable airway IL-33 levels were observed in CS and FS with stable or exacerbating COPD. Results suggest potential benefits of inhibiting IL-33red and IL-33ox activity in CS and FS with COPD. Tozorakimab, an anti-IL-33 mAb with a dual mechanism of action inhibiting IL-33red and IL-33ox activity, is being investigated in Ph 3 studies in COPD ( NCT05166889 , NCT05158387 , NCT06040086 , NCT05742802 ). 1. Steiling K et al. Am J Respir Crit Care Med 2013;187:933–42. erj;66/suppl_69/PA6356/F1 F1 F1

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