Interleukin 33: a suitable target for biological therapies of COPD?

Abstract

Extract COPD is a progressive and disabling lung disorder characterised by poorly reversible airflow limitation and mucus hypersecretion, associated with dyspnoea, low exercise tolerance and poor quality of life [1]. Indeed, COPD is one of the main causes of morbidity and mortality worldwide, as well as the most common determinant of chronic respiratory failure [2]. Available pharmacological strategies that are currently used for COPD treatment include bronchodilators and inhaled corticosteroids [3]. However, although these treatments can improve symptoms and decrease exacerbation rate, they do not appear to be able to effectively suppress the underlying pathogenic processes. Among these, smoking-driven oxidative stress and airway inflammation play a key role [4]. In particular, inflammatory mechanisms involve the active participation of the innate immune system, as shown by accumulation within the airways and lung tissue of neutrophils, macrophages, innate lymphoid cells, dendritic cells, natural killer cells, and sometimes also eosinophils and mast cells [5].