Role of the inflammasome in chronic obstructive pulmonary disease (COPD)

// Chiara Colarusso 1 , Michela Terlizzi 1 , Antonio Molino 2 , Aldo Pinto 1 and Rosalinda Sorrentino 1 1 Department of Pharmacy, University of Salerno, ImmunePharma s.r.l., Fisciano, Salerno, Italy 2 Department of Medicine and Surgery, Respiratory Division, University of Naples “Federico II”, Naples, Italy Correspondence to: Rosalinda Sorrentino, email: // Keywords : inflammation, COPD, lung injury, immune response, inflammasome, Pathology Section Received : January 31, 2017 Accepted : April 19, 2017 Published : May 13, 2017 Abstract Inflammation is central to the development of chronic obstructive pulmonary disease (COPD), a pulmonary disorder characterized by chronic bronchitis, chronic airway obstruction, emphysema, associated to progressive and irreversible decline of lung function. Emerging genetic and pharmacological evidence suggests that IL-1-like cytokines are highly detected in the sputum and broncho-alveolar lavage (BAL) of COPD patients, implying the involvement of the multiprotein complex inflammasome. So far, scientific evidence has focused on nucleotide-binding oligomerization domain-like receptors protein 3 (NLRP3) inflammasome, a specialized inflammatory signaling platform that governs the maturation and secretion of IL-1-like cytokines through the regulation of caspase-1-dependent proteolytic processing. Some studies revealed that it is involved during airway inflammation typical of COPD. Based on the influence of cigarette smoke in various respiratory diseases, including COPD, in this view we report its effects in inflammatory and immune responses in COPD mouse models and in human subjects affected by COPD. In sharp contrast to what reported on experimental and clinical studies, randomized clinical trials show that indirect inflammasome inhibitors did not have any beneficial effect in moderate to severe COPD patients.