Introduction

Inflammasomes have recently been identified to be critical and potent inducers of inflammation that when overactive may be targeted therapeutically in inflammatory diseases. Inflammasomes are multiprotein signalling complexes that control the maturation and release of pro-inflammatory cytokines in response to numerous exogenous, endogenous and pathogenic danger signals (figure 1).1 They mediate host responses, particularly interleukin (IL)-1β release and neutrophilic inflammatory responses, which are essential for protection against infection. However, recent evidence demonstrates that excessive inflammasome activation is a feature of numerous inflammatory diseases including COPD, neutrophilic asthma, idiopathic pulmonary fibrosis, cystic fibrosis, acute respiratory distress syndrome (ARDS) and respiratory infections (table in figure 1). Infections are the most widely recognised activators of inflammasomes; however, this field has recently been reviewed extensively and is beyond the scope of this article. Their roles in ARDS and potential for therapeutic targeting are well established.2 It is now emerging that inflammasomes are likely involved in the pathogenesis of COPD and asthma, and further investigation is urgently needed.